Dr. Stuart Reichler’s Fall Bio 325 Homework #2
Should be emailed to sreichler @ mail.utexas.edu by Tuesday, October 10th at 11am

    We (students, professor, and TA) are going to work together to determine the topics we will study for the latter part of the class.  Now that each of you have submitted an article that you feel would be worthwhile to study, we are all going to work together to decide which articles we will cover.  Please email me your top 5 choices, numbered from 1 (favorite) to 5 (fifth favorite), and a short, less than 100 words description of why you chose each of these five article.  Your rationale for choosing the articles should include why you think it is important for us to study these topics, and/or why you think the topics are interesting.  The articles are listed below.

    The format of the assignment should be as follows:
Your name
Bio 325

1) Favorite:  Article title
This is my favorite article because...

2) Second Favorite:  Article title
This is my second
favorite article because...

3) Third Favorite:  Article title
This is my third
favorite article because...

4) Fourth Favorite:  Article title
This is my fourth
favorite article because...

5) Fifth Favorite:  Article title
This is my fifth
favorite article because...

    Please include your assignment in the body of an email and send it to me by 11am on October 10, 2006.  This homework will be graded on a scale of 0-3 points based on your rationale for choosing the five articles.  I will subtract 0.5 points for each day late.  After I receive all of your submissions, I will post the schedule for the rest of the semester.

Articles: in no particular order:

Article Title: The Genetic Architecture of Sucrose Responsiveness in the Honeybee ( Apis mellifera L.)

Authors: Olav Rueppell, Sathees B. C. Chandra, Tanya Pankiw, M. Kim Fondrk, Martin Beye, Greg Hunt, and Robert E. Page

Journal Title: Genetics

Volume: 172, Issue 1, January 2006

Page Numbers: 243-251

Date of Publication: January 2006


The chief question posed in this study regards the way in which genetic architecture affects behavioral syndromes through the study of the pollen-hoarding syndrome of the honeybee Apis mellifera L. Being a psychology major myself, I feel that social behavior is influenced by two kinds of factors - environmental factors, and biological factors. Through a perspective involving genetics, this article clarifies the importance of the understanding of behavioral syndromes through the understanding of genetic architecture, and combining the realms of biology and psychology, emphasizes how this knowledge mixes to give us a clearer understanding of "social evolution". By gaining better insight into the biological and genomic system of the pollen-hoarding synrdome of the honeybee, we may be enlightened in our future endeavors towards understanding not only psychological and neurological pathways, but also studies of "naturally occurring behavioral syndromes". The study of the honeybee's pollen-hoarding syndrome is considered to be a "hard-wired" trait, and to the authors knowledge, is "the first study of genetic architecture of a behavioral reflex". Personally I feel that this article not only gives us more insight into the fields of biology (genetics), I believe that it also stimulates interest into the unknown and dark realm of behavioral psychology, ( i.e. how we behave, and why we may be predisposed to behave in (a) certain manner(s)).

Title: Live Bacterial Vaccines- a review and identification of potential hazards
Author’s Names: Ann Detmer and Jacob Glenting
Journal Title: Microbial Cell Factories
Volume 5, Article 23
Date Published: June 23, 2006

Questions Posed:

• What are the advantages of using live bacterial vaccines/ disadvantages?
• What could be the effects caused by the release of the recombinant DNA into
• What should you consider during the development of these vaccines?
• What methods are already available, how are scientists going to go about
finding new methods?

What makes this article interesting?

This article gives the history of the use of bacterial vaccines, which dated
back to the late 1800’s, but was not a useful tool until the 1980s. The first
uses of this method failed due to the sequence reverting back to the harmful
strain. This article also explains what can make a safe vehicle for the
delivery of a vaccine; it also lets the readers know the aspects other than
science that need to be considered, such as cost efficiency and patient
comfort. The article also describes how these pathogens can be made safe for
intake; they mutate the genes that encode for enzymes or delete harmful
factors, some strains are even created so that they may not be replicated
inside the human body.
The article describes how they test the DNA of the patients to see if the
vaccine has entered the chromosome of the human. In this case they use PCR
(polymerase chain reaction) to sequence the DNA. They can then also test how
this insertion affects the rest of the gene activity of the organism.
This article explains how the use of the study of Genetics can lead to
preventing diseases and immune deficiencies. It also explains why methods of
sequencing are so important in the world today, not just to figure out the
genome of an organism, but to also learn how genes can be affected by the
environment as well as attempts to remove disease will affect the genes and the
way information is coded.

ARTICLE TITLE: Highly efficient EIAV-mediated in utero gene transfer and expression in the major muscle groups affected by Duchenne muscular dystrophy

AUTHORS' NAMES: Gregory LG, Waddington SN, Holder MV, Mitrophanous KA, Buckley
SMK, Mosley KL, Bigger BW, Ellard FM, Walmsley LE, Lawrence L, Al-Allaf F,
Kingsman S, Coutelle C, Themis M

SOURCE: Gene Therapy, Volume 11, Issue 14, Pages 1117-1125, July 2004

Duchenne muscular dystrophy (DMD) is an X-linked genetic disorder
characterized by degeneration of the skeletal muscles. Post-natal gene therapy
for this disease has currently proved unsuccessful due to immune response
against the treatment and the inability to provide widespread gene transfer.
The authors of this article attempt to determine whether such obstacles can be
overcome by administering gene therapy prenatally as a cure or treatment method
for DMD.
In an attempt to answer this question, researchers designed an experiment
in which mouse fetuses were injected with a virus that would provide gene
transfer to the various muscle groups affected by DMD. The fetuses were then
analyzed based on the number of injections they had received and the site of
the injections. Results indicated that, even after a single injection, there
was widespread gene expression in the various muscles of the fetuses, including
the heart, diaphragm, liver, and limbs. In addition, many of the complications
associated with post-natal gene therapy, particularly rejection of the
treatment by the immune system and the inability to reach several muscle
groups, were absent in this pre-natal approach.
In recent years, Duchenne muscular dystrophy has received worldwide
attention, especially through the annual Jerry Lewis fundraising telethon.
Most DMD patients live only to be 20 or 30 years old, and there is presently no
cure for this fatal disease. While gene therapy is a relatively new field in
modern medicine, it is being sought as a potential treatment for currently
incurable diseases. The authors of this article present us with supporting
evidence that pre-natal gene therapy may one day provide a method of preventing
or treating DMD. If so, this would certainly be a significant breakthrough in
the scientific community.

How does the mode of inheritance of a genetic condition influence families? A
study of guilt, blame, stigma, and understanding of inheritance and
reproductive risks in families with X-linked and autosomal recessive diseases,
James, Cynthia A. ScM, PhD1; Hadley, Donald W. MS2; Holtzman, Neil A. MD, MPH3;
Winkelstein, Jerry A. MD3, The American College of Medical Genetics Volume
8(4), pp 234-242, April 2006.

They basically surveyed families with genetic disorders and asked them questions
about their knowledge of inheritance and reproductive risk; their concern for
future family-members; their feelings of guilt and blame and stigmatization.
I think it is interesting because it focuses on the people that have genetic
disorders and how they feel about possibly passing these genetics disorders on
to their family.

"Reversal of Type 1 Diabetes by Engineering a Glucose Sensor in Skeletal
Muscle." Alex Mas, Joel Montane, Xavier M. Anguela, Sergio Munoz, Anne M.
Douar, Efren Rui, Pedro Otaegui, Fatima Bosch. Vol. 55, issue 6. p1546-1553.

This article focuses on the use of gene therapy, a relatively new and innovative
domain in science aimed to manipulate genes to solve health problems.
Researchers used gene therapy, specifically the AAV1 vector, to solve
implications with diabetes type one. The greatest problem in diabetes type 1
patients is the inability of the body to maintain normoglycemia due to a
defective pancreas. Traditional treatments focus on performing the pancreas’s
duty, by manually injecting needed insulin only in response to blood sugar
fluctuations. A secondary complication occurs when the basal rate, in between
meals, of blood sugar levels cannot be achieved. Researchers wanted to find out
if insulin uptake areas, like skeletal muscles, would be a better area to
manipulate to not only basal rate normoglycemia and prevent secondary
complications. They tested mice by injecting them with AAV1 gene vectors to
pair with glucokinase to regulate insulin uptake from the blood stream to
skeletal muscle. Essentially, researchers found that the vector paired with
the glucose enzyme could in fact turn on and off insulin uptake and ultimately
achieve normoglycemia. Their results posed the question of whether this
procedure in mice could be replicated in humans and achieve the same results.
Experimenters would like to use larger mammals to test applicability in humans
and any safety concerns. The alternative perspective to treat the uptake area
instead of focusing on the outtake area is a major advance in treatment of all
health issues. Success from this experiment will hopefully encourage other
researchers to use gene therapy along with a holistic treatment plan approach
to solve issues in new and creative ways. Diseases and defects affect vast
ranges of functions due to the complexity and systematic nature of the human
body. Could gene therapy thus be used to enhance the works of one area of a
system to combat the problems from another area of that system? If the answer
is yes, as this experiment has supported, then many unanswered questions in
medicine may could start to be answered.

Müller, U. F. "Re-creating an RNA world." Cellular & Molecular Life Sciences 63.11 (2006): 1278-1293. Academic Search Premier. 9 September 2006.
Description of the Article
The article talks about the RNA World Hypothesis. The RNA world hypothesis proposes that RNA was the first life-form on earth, later developing a cell membrane around it and becoming the first prokaryotic cell. The RNA World hypothesis is supported by the RNA's ability to store, transmit, and duplicate genetic information, just like DNA does. RNA can also act as a ribozyme (an enzyme made of ribonucleic acid). Because it can reproduce on its own, performing the tasks of both DNA and proteins (enzymes), RNA is believed to have once been capable of independent life. But the RNA World Hypothesis has not been fully proved true yet. After giving a short background on prebiotic chemistry and in vitro evolution, the discussion focuses on the generation of three important components of an RNA world: a sufficient polymerase ribozyme, self-replicating membrane compartments and ribozymes that are capable of performing basic metabolic processes. The article proposes that synthesis of self replicating system from the catalytic RNA would be a milestone in the search for the origins of life and for our understanding of life itself. Some steps like modification of several existing ribozymes along with the development of new ribozymes have been taken and very soon there would a development of a self replication system from RNA. This would prove that RNA world hypothesis is true.
Reason to study the article in clas
This article could be used for class study and discussion due to several reasons. Firstly, the topic is related to our curriculum and we have briefly talked about this in the class. Secondly, the article provides some updates on what research work is going on and what progress has been made to prove that RNA world hypothesis is true. If we can prove that life originated from RNA then the whole perspective of functions and structures of proteins, DNA and RNA will be changed. Also, many myths and misunderstandings regarding the origin of life can be disregarded if this study is successfully conducted. Origin of life is one the most interesting and important part of biology and there it should be studied in detail in the class.

Genome-wide linkage analysis of heroin dependence in Han Chinese: Results from wave one of a multi-stage study.
Stephen J. Glatt, Jessica A. Su, Shao C. Zhu, Ruimin Zhang, Bo Zhang, Jixiang Li, Xiaobo Yuan, Jianhua Li, Michael J. Lyons, Stephen V. Faraone, Ming T. Tsuang. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. Volume 141B, Issue 6, p 648-652 (5 September 2006). Published Online: 19 Jul 2006.

Heroin addiction is a worldwide epidemic with its use on the rise. Genetic
contribution seems to be higher for heroin addiction than any other illicit
drug; previous studies suggest that genes account for between 23 and 54% of
total liability of heroin dependence. Even though gene association studies
have been performed, the specific genes that govern this heroin dependence
remain unknown. This article describes a study where researchers try to find
out which, if any, specific genes control heroin dependence; this is the
question being asked.
Researchers used people from the Yunnan Province in China as their study
subjects. People with siblings or other family members were asked to
participate in this experiment and the family member was also evaluated for
possible inclusion in the study. Blood from the subjects was drawn, and DNA
was extracted from cell lines and genotyped. Computer programs were used to
collect data on genetic markers and there were two areas of interest that
seemed to link to heroin addiction.
I chose this article because it seemed very relevant to our study of genetics in
several ways. The purpose of learning about genetics is to be able to use what
we know and apply it to some good use. This article shows just that:
researchers trying to identify genes responsible for a dangerous drug
addiction. This also ties into our discussion of nature vs. nurture. These
researchers say that dependence is largely based on genetic characteristics.
However, while they have positive proof in that they found two loci having
suggestive evidence for linkage, they don’t do much to disprove the
environmental influence since the source of these subjects came from an area
that produces more than 20% of the world’s heroin. They do show weaknesses in
their study as well as their plans for further studies in linking the loci to
heroin dependence. Overall, they carried out the rules of strong inference:
they devised a hypothesis, designed an experiment, carried out the experiment,
and they will repeat the experiments with refined approach based on their

Article Title: Anthrax lethal factor and edema factor act on conserved targets
in Drosophila.

Authors: Annabel Guichard, Jin Mo Park, Beatriz Cruz-Moreno, Michael Karin, and
Ethan Bier

Journal Title: Proceedings of the National Academy of Sciences of the United
States of America

Date: February 23, 2006

Volume: 103

Issue: 9

Pages 3244-3249
(DOI: 10.1073, PNAS: 0510748103)

Summary: The article talks about an experiment that these authors did to see if
the toxin, Anthrax, has similar effects in a Drosophila (fruit fly) as in
humans. If the experiment proves to be successful, researches will be able to
use fruit flies in experiments to better understand the effect of toxins in
humans. Anthrax secretes three exotoxins, a lethal factor, edema factor, and a
protective antigen. Each of these exotoxins may cleave or inhibit different
genes in the development of the fruit fly. The results show that anthrax poses
similar development effects in fruit flies as in humans.

Reason: It is important for us to look at an article like this, because humans
can be exposed to different toxins at any moment, and we should understand how
these toxins work in our body. We need to understand how they inhibit or their
activities in gene expression in the human body or any other animal.

Excess of counterclockwise scalp hair-whorl rotation
in homosexual men
By Amar J. S. Klar, Journal of Genetics, Vol. 83, No.
3, pages 251-255, December 2004

The article I chose deals with the question of a
person's sexual preference. Is it innate, learned or
due to a combination of both? This article looks at
the direction of scalp hair-whorl rotation
development from a common genetic mechanism and
whether or not this same mechanism specifying mental
makeup influences sexual preference. I think this
article would be interesting to discuss in class
because this is a highly debated topic, is sexual
orientation nature or nurture. We touched a little in
class already but this article exams another
similarity between homosexual men that isn't commonly
found in heterosexual men.

The role of microRNA genes in papillary thyroid carcinoma, Huiling He, Krystian
Jazdzewski, Wei Li, Sandya Liyanarachchi, Rebecca Nagy, Stefano Volinia, George
A. Calin, Chang-gong Liu, Kaarle Franssila, Saul Suster, Richard T. Kloos, Carlo
M. Croce, and Albert de la Chapelle, Proceedings of the National Academy of
Sciences of the United States of America, vol. 102, 19075-19080, December 27,

The questions posed in the article are “What is the role of microRNA in
papillary thyroid carcinoma (PTC)?” and “What causes predisposition for PTC?”
MicroRNAs, previously thought of as “junk” DNA in the genome, were only
recently recognized as a class of gene products. Scientists know that some
people inherit predispositions for PTC and their attempts at finding specific
gene mutations for this predisposition have been unsuccessful (eliminating one
of the hypothesis explaining what causes predisposition of PTC). Because of
these unsuccessful previous attempts, these researchers hypothesized that
microRNA were involved with the predisposition for PTC and that they worked as
regulatory genes instead of protein-producing genes. The research suggests that
the predisposition to PTC is caused by a subtle interaction among many genes
instead of just one. After comparing samples from malignant tumors and healthy
cells adjacent to the tumors, researchers concluded that several miRNA types
were overregulated while transcript and protein from other genes were
down-expressed. Specifically, the scientists found that when three dramatically
overexpressed miRNA types were found in the presence of two other miRNA types,
the cell would become cancerous. This article would make for an interesting
class because it would show a genetic cause behind the correlation between
family cancer history and a person’s chance of getting cancer.

Blood group A and B antigen expression in human kidneys correlated to
A(1)/A(2)/B, Lewis, and secretor status, Breimer ME, Molne J, Norden G, Rydberg
L, Thiel G, Svalander CT, TRANSPLANTATION, volume: 82 issue: 4 pg:479 -485, AUG
27, 2006

This article attempts to solve the problem of ABO blood type barriers.
Transplantation of organs cannot be made among people with different blood
types. In this study, the three types of blood are studied, revealing three
different groups of blood, with major, minor and minimal antigen expression
patterns. It categorizes the donors into A1, A2, B, with Lewis and secretor
status, corresponding them into three different intensities designated as 3+,
1+, and +. Drug treatments were used to test the organ biopsies as well, and
the results indicate an insufficiency to use pretransplant antibody removal and
standard immunosuppressive drugs as the only pretreatment to transplantation.
ABO blood incompatibility occurs despite splenectomy, and whether to use
anti-CD20 antibodies instead of Splenectomy will increase the long-term graft
survival in renal transplantation remains to be further studied.

This is an interesting article in the sense that blood transfusion barriers have
always been present and accepted. Scientist now are reviving an interest in the
differences in these blood types, and trying to find a way to cross the ABO
barriers in organ transplantation.

Pollard, K. S., Salama, S. R., Lambert, N., Lambot, M., Coppens, S., Pedersen, J. S., Katzman, S., King, B., Onodera, C., Siepel, A., Kern, A. D.,
Dehay, C., Igel, H., Ares, M., Vanderhaeghen, P. and Haussler, D. 2006. An RNA gene expressed during cortical development evolved rapidly in humans. Nature, 443: 167-72.
Pollard et al. studied the genomic regions in humans and identified the regions that have a significantly accelerated rate of substitution compared to that of the chimpanzee. They found that one of the most dramatically accelerated regions is an RNA gene (HAR1F), which is expressed in Cajal-Retzius neurons in the human neocortex early in human embryonic development. HAR1F was detected along with reelin protein which showed that both HAR1F and reelin are expressed in the same cells. One question remaining is about the role of HAR1F and HAR1R in cortical development and whether or not HAR1F directly or indirectly influences the expression of reelin or its receptors. These human accelerated regions (e.g. HAR1F) are one of the focuses in the attempt to decode the key events of human evolution.

“Generations of Cloned Transgenic pigs in omega-3 fatty acids.” Jing Kang.
Nature Biotechnology. Volume 24 (435-436). Published April 2006.

This article would make an interesting topic because it is a very controversial
one. For one, the transgenic pigs were cloned via nuclear transfer. Cloning
is a major thing many people despise mainly for religious and ethical reasons.
However, as a class, we should put our scientific coats and think thoroughly
whether current meat should be replaced with “hfat-1 transgenic pig.” The
latter meats may reduce the prevalence of heart disease, cancer, diabetes,
arthritis, and depression.

Genetic engineering is advancing, and so are the food prices. Should the vast
population be fed with minute amounts of organic goods that require a lot of
labor, or should genetic engineering contribute largely to the quality and
quantity of food?

Organic food is expensive. Generation of fat-1 transgenic livestock may be an
economical and sustainable choice. Studying these types of articles will lead
give us a better understanding of transgenes, its benefits and its defects.

A Study of Identical Twins' Palmprints for Personal Verification; Adams Wai-Kin
Konga, David Zhanga, and Guangming Luc; Pattern Recognition; volume 39; issue
11; pages 2149-2156; November 2006. (available online June 16, 2006)

This experiment attempts to discover if identical twins' palmprints can be used
for identification purposes. In other words, it answers the question: are
identical twins' palmprints identical or different? The device used to examine
the palms was referred to as an "automatic palmprint identification algorithm,"
and it was able to distinguish the different line patterns on identical twins'
hands. The results of the experiment show that the three main lines and other
larger lines on two identical twins' hands are genetically the same. However,
smaller lines differ between twins, showing that nature and nurture both play
roles in determining the lines on a person's hand. Therefore, palmprints are
unique to each individual and can be used to identify people, even identical
twins. I think this article would be interesting to study because it goes along
with what we have been learning in class about nature and nurture. It also
supports the idea that they work together, instead of one being completely
dominant over the other.

"Paternally inherited HLA alleles are associated with women's choice of male
odor", Suma Jacob, Martha McClintock, Bethanne Zelano, & Carole Ober, Nature
Genetics, Volume 30 No 2, pp 175-179, published January 22, 2002

This article describes the ability for women to detect difference of one human
leukocyte antigen (HLA), or human MHC, among male odors even though background
odors which are influenced by cultural practices and the rest of the genome my
mask the olfactory cues. The ability for women to discriminate and choose odors
is based on the HLA alleles she has inherited from her father and not her
mother. The data shows that the paternally inherited HLA-associated odors
influence odor preference, or in other words, who she may or may not be
attracted to. There is not one male odor that is preferred among everyone, most
women prefer different odors. This article is interesting because it plays on
the saying that women are attracted to men with qualities similar to their
fathers. In retrospect this is true because the alleles for this ability are
inherited by their father but actually the tests show that women are attracted
to men with HLA alleles most unlike their own. So, in my opinion, it is saying
that women are attracted to men that are the opposite of their fathers. This
article sparked an interest in me because it showed, for the most part why
women are attracted to certain types of men. I think other females and maybe
some males in this class would be interested about it as well. Maybe one day we
will be able to skip dating and go straight to their DNA to see if they would
suit us or not.

Title: Tetracycline-Regulated Gene Expression in Replication-
Incompetent Herpes Simplex Virus Vectors



Volume and Page numbers: 13:2113–2124

Date of publication: December 10, 2002

This article adresses Herpes Simplex Virus vectors ability in gene delivery, and regulating the gene expression in these vectors. This vector is used frequently in the gene delivery to the neuron and the nervous system. Herpes simplex virus normally infects human neurons and naturally establishes a latent state in which the viral genome persists in a nonintegrated form, without apparent disruption of neuronal function. These characteristics, and the ability of the vector to be engineered to accommodate large inserts of foreign DNA, make HSV an especially attractive vector for studying the central nervous system and the neuron, as well as a potential gene therapy vector. The main purpose of this study is to make modifications to expand the range and sensitivity of inducible gene expression in the HSV vector system, so that it can be used to turn gene expression on and off in the ireplication-incompetent herpes simplex virus vectors to be used in neuron like cells.

Rapid Communication: Serotonin Transporter Promoter Polymorphism and Differences
in Alcohol Consumption Behavior in a College Student Population, Depetrillo,
Paolo B., Vasilopoulos, Nicholas L, Philbeck, John W., Herman, Aryeh I.,
Alcohol and Alcoholism, 38, 446-449, 2003.

Alcohol misuse is generally associated with the depiction of the
college life. An individual’s first drink away from home usually occurs in
their college years, in a social setting, at a party, or at a club. Those
first few drinks may not seem like such a big deal until they unravel into the
fatal potential of binge drinking. The purpose of this study is to explore
what leads college students to binge drinking or drinking to get drunk, and if
they are caused by genetic factors that support this type of behavior.
Alcohol misuse is an increasing problem among college campuses today when
students are found unconscious on the couch from alcohol poisoning, individuals
are being killed on the street by drunk drivers, and people’s children are found
left to die after a Frat Pledge Party. Researchers have found that there are
differences in the serotonergic functions deliberated by the serotonin
transporter protein promoter polymorphism (5-HTTLPR) among college students,
which may give rise to explaining why some students have a greater tendency to
drink than others do. The most common type of insertion deletion polymorphisms
lies in the promoter area in the human 5-HTT gene, and lays the foundation to a
long allele (L) as well as a short allele (S). The higher the frequency of
this S allele may suggest a higher ethanol tolerance and alcohol self
–regulation for adults that are 26 years old or younger. Individuals who were
homozygous with the S allele in a group of adult alcoholics had a higher
frequency of binge drinking than those who were did not carry the S allele, or
S homozygous.

262 college-aged participants of Caucasian, Asian, African-American, and other
ethnic descents answered a survey questionnaire using an ordinal scale. The
participants were also genotyped for the 5-HTTLPR gene for further genetic
examination. The survey asked questions such as “On how many occasions have
you had a drink of alcohol in the past 30 days?” or “Think back over the last 2
weeks. How many times have you had five (for male students) four (for female
students) or more drinks in a row?”, and a drink of alcohol was operationally
defined as a 12-ounce serving in a can or a bottle, or a 4-ounce wine glass.
The survey also answered questions such as whether the student was a binge
drinker, who drinks dangerously excessive amounts of alcohol in one sitting, or
a student who drinks purposefully just to get drunk.

The Caucasian population of the participants, 204 out of the 262
participants, were the only group further analyzed in the results to avoid
ethnic comparison. This is not a study of which ethnic group can get more
smashed on a Saturday night, it is a study of the gene that some people possess
and how it is significant in their behavior around alcohol.

Researchers did match their predictions as the results do suggest a
major association with the 5-HTTLPR gene with an increase in alcoholic behavior
and consumption in Caucasian participants. Those students who were homozygous
for the S allele of the 5-HTTLPR had the highest frequency of drinking more
often to get drunk, as well as binge drinking. Those students who were
heterozygous for the S allele, or were homozygous with the L (long) allele had
a lower tendency to drink excessively. This study poses the finding that
individuals with the homozygous S allele may use alcohol to reduce stress, as
these individuals showed greater levels of anxiety. Nonetheless, this study
does reveal that 5-HTTLPR does have an impact on drinking behavior, and also
increases our knowledge about the genetic risk that we should be aware of to
protect ourselves and our loved ones.

The Cells and Logic for Mammalian Sour Taste Detection, A. L. Huang, X. Chen, M.
A. Hoon, J. Chandrashekar, W. Guo, D. Trankner, N. J. P. Ryba & C. S. Zuker,
Nature, Volume 442, pp 934-938, 24 August 2006.

Have you ever thought about what happens when you put something in your
mouth and taste it? What exactly does it mean to taste something sweet or sour?
And why have we evolutionarily developed these tastes? This article not only
explains the mechanism that lets us taste “sour,” but also uses the findings
from that experiment to research the pH sensitivity of cerebrospinal fluid.
We all have five basic tastes: sweet, sour, salty, bitter, and umami (the
flavor of MSG). I never really understood or even questioned what tasting a
certain flavor meant. Was the same “thing” that told my brain I was tasting
sweet, the same “thing” telling my brain I was tasting sour? Apparently not.
The scientists working on this project determined that PKD2L1 (a
polycystic-kidney-disease-like ion channel), what they proposed as the
candidate for the mammalian sour taste detector, was expressed in taste
receptor cells (TRCs) distinct from the TRCs responsible for the other tastes.
Basically, this ion channel that correlated with “sourness” was activated in
certain taste cells independently from the other tastes that could be
Furthermore, when mice were genetically engineered to have these certain
populations of TRCs removed, (the ones that expressed PKD2L1), the mice were
completely devoid of taste responses to sour stimuli! This shows that without
these PKD2L1 expressing cells, the mice could not taste (respond) to sour
stimuli. But the capacity to respond to the other tastes (sweet, bitter…) was
unaffected. Not only did this show that PKD2L1 expressing cells were the only
ones responsible for tasting sour, but it also showed that the 5 different
tastes were distinct and independent from each other. The article provides
helpful figures and diagrams to help understand this.
From previous work in isolating the receptors for sweet, bitter, and umami, the
scientists were able to show that each of the 5 tastes were mediated by, “highly
selective receptor proteins expressed in distinct and independent populations of
TRCs.” From this conclusion, they came up with the hypothesis that sour taste
should also be mediated by these highly selective, distinct, and independent
Since I didn’t know much about how something that goes into our mouth and onto
our tongue actually gets registered in our brain as either sweet or bitter or
sour, I thought it was interesting to find out what exactly is happening on our
tongue. In mammals, TRCs have specialized microvilli that project out into the
taste pores. It’s in these pores that the interaction between “tastants” and
our taste receptor proteins occur. These TRC compartments are actually the
only place taste receptor proteins function! From this information, the
scientists hypothesized (correctly so) that since the receptor proteins were
located here, the receptors themselves should also be located in these taste
Since PKD2L1 was found to be involved in detecting and responding to pH levels,
another interesting question evolved from these conclusions: Was PKD2L1
expressed in cells elsewhere in the body for this same function? Other than in
the taste receptor cells of the tongue to detect sourness (implying higher
acidity and lower pH levels), PKD2L1 was also found in neurons surrounding the
central canal of the spinal cord! (Another helpful figure is provided to show
the localization of PKD2L1 expressing cells around this region.)
Because PKD2L1 was known for detecting pH changes, these scientists came up
with another hypothesis predicting that, “these cells might be part of the
homeostatic circuitry responsible for monitoring and reporting the pH of the
CSF…that these neurons should trigger action potentials in response to acid
stimulation.” Their hypothesis was correct, for they found that when they
genetically engineered mice to have fluorescently labeled PKD2L1 in CSF cells,
and then varied the pH levels, there was a marked increase in the action
potential frequency of these labeled cells (but not in the cells without
PKD2L1). A few charts and visual representations are also provided here to
explain the action potential firing in response to pH stimulation.
So, after learning that PKD2L1 functions as a sort of indicator of pH levels,
it was interesting to see how the ion-channel can be found in two completely
different parts of the body for similar reasons. In the tongue, PKD2L1 is
necessary to detect sour tastes, thereby preventing mammals from eating highly
acidic foods that may be rotten or spoiled. While in the fluid of the spinal
cord, it’s used as a sensor to indicate the pH variations of the CSF, (since
any slight deviations from a pH of 7.4 within the body could be detrimental.)
As the article more eloquently states, “… [it’s] a surprising unity in the
cellular basis of pH sensing in very different physiological systems.”

Effect of Long-Term Somatotropin Treatment on Body Composition and Life Span in
Aging Obese Zucker Rats, Michael J. Azain, J. Roger Broderson, and Roy J.
Martin, Experimental Biology and Medicine 231 (1): 76-83, 2006

This research tested the effect of the growth hormone STH (Stomototropin) on fat
composition in rats. It also tested the life span of rats compared to the
percentage of fat in their bodies. The growth hormone STH stimulates more
uptake of food but increases the amount of lean tissue and decreases fat. In
humans it has been found that there is a direct effect of increase body fast on
dying. The more fat content one has the more likely he/she is to die at an
earlier age. A decrease in hormone is proved to lead to an increase in body fat
content. It has been found that STH works as an anti-aging substance. The more
growth hormone one has the longer he/she will live.

For the first experiment, the researchers tried to determine if STH had an
effect on growth and body fat content. They had both male and female lean and
obese rats. Some were given STH and others were not. The beginning body weights
of the lean rats were about the same. The obese rats all had about the same
weight as well. They determined the fat composition and weighed certain organs
to see the effect of STH. For the second experiment, they tested to see if a
decrease in body fat did cause the rat to live longer. This was again done on
male, female, lean and obese rats.

The overall significance of this article is to show that fat percentage in the
body does have a substantial effect on life span. The more fat percentage you
have the shorter your life span. It also shows that one hormone, STH, cannot
fix the problem of obesity. Many different factors including exercise and a
balance diet are essential to having low fat percentage. People are always
trying to find an easy way out of their problems such as one pill to make them
be skinny. This shows that just an increase of STH does not have the best
effect. Although it may lower fat composition, the obese mice lived an even
shorter life. It is important to find a balance. The STH affected the renal
organ in mice. Increased hormones in humans may have the same negative effect
on other organs. I found this to be very interesting. Currently with the diet
craze and professional athletes using growth hormone, I think it is interesting
to learn how steroids do affect the body and fat composition.

Title: “Extreme skewing of X chromosome inactivation in mothers of homosexual
Authors: Sven Bocklandt, Steve Horvath, Eric Vilain, and Dean H. Hamer
Journal: Human Genetics
Volume: 118 Pg. 691-694 Feb. 2006

The issue of nature versus nurture has been an ongoing debate for many years.
Topics such as a child’s language development are generally considered by many
to be influenced by both nature and nurture; however, a person’s sexual
orientation is almost never regarded as one of these topics. Most would state
that a person’s sexual orientation is strictly due to environmental factors.
Recent researches, however, have indicated that a person’s sexual orientation
might be influence by genetic. To test whether sexual orientation is related to
genetic, researchers gathered a sample of mothers of heterosexual men and a
sample of mothers of homosexual men. Researchers tested the genetic information
of both samples of mothers and found that mothers of homosexual men have
statistically more extreme skewing of X chromosome inactivation than mothers of
heterosexual men.

In a female, each cell has two X chromosomes, but one X chromosome is randomly
inactivated into a barr body. Because the process is random, the distribution
of cells in the female body having one particular inactive X chromosome should
be close to 50 percent. Extreme skewing of X chromosome inactivation is the
phenomenon in which one particular X chromosome is found to be inactivated in a
very large percentage of the cells in the body. Researchers believe that extreme
skewing of X chromosome inactivation is due to the cells having some sort of
bias for one X chromosome over the other; however, researchers have very little
information on the cause of this bias. After the researchers gathered and
analyzed the data, the results showed that there is a significant increase in
extreme skewing of X chromosome inactivation in mothers with homosexual sons
compared to mothers with heterosexual sons. The result becomes even more
significant in mothers of two or more homosexual sons. Though this research
does not relate to mothers of homosexual females nor does it prove that sexual
orientation is caused by genetic, it does provide some evidence relating sexual
orientation and genetic.

This article would be very interesting to discuss in class because it provides a
different perspective on homosexuality. If sexual orientation is influenced by
genetic, then homosexuality can be considered a genetic disorder like Down
Syndrome. As researches continue to provide more information, the debate
regarding the relationship between sexual orientation and genetic will continue
to increase; therefore, our class should take this opportunity to discuss this
topic and debate whether homosexuality should be considered a disease if it is
found to be influenced by genetic.

Title: Potent inhibition of HIV-1 gene expression and TAT-mediated apoptosis in human T cells by novel mono- and multitarget anti-TAT/Rev/Env ribozymes and a general purpose RNA-cleaving DNA-enzyme
Author: Hoshang Unwalla, Samitabh Chakraborti, Vikas Sood, Nidhi Gupta and Akhil C. Banerjea
Journal: Antiviral Research
Volume 72, Issue 2 , November 2006, Pages 134-144
Questions: How and by what mechanisms is it possible to reduce the HIV-1 TAT protein created in HIV infected cells and what real effects would it have when in the real human body (not in vitro)? Could this, at some point, become a plausible treatment for HIV?
I think that this is a great article review because it shows great genetic insight to the functioning of one of the deadliest viruses in the world right now. It also offers an experimental treatment to the HIV virus which may be complicated yet covers many of the core topics of genetics.

Minoo Rassoulzadegan, et al., "RNA-mediated non-mendelian inheritance of an epigenetic change in the mouse." Nature, Volume 441,
p469-474, 25 May 2006. 17 August 2006

DNA has long been thought as the sole carrier of information from one generation to the next. However, a study by
a team led by Minoo Rassoulzadegan at Sophia Antipolis University in Nice, France, conclude that RNA as well as DNA
can carry information from parent to child. This is a clear contradiction to Mendel's law of inheritance stating that the combination
of dominant and recessive genes dictate the offspring's characteristics. The dominant mutant gene Kittm1Alf results in a spotted tail
and the normal Kitgene codes for a brown tail. A mouse with two normal copies of the gene, and a mouse with one Kittm1Alf gene
were then bred.  However, mice that inherited two normal copies of the gene also had spotted tails.
When the team examined sperms from males carrying one normal and one mutant copy of the Kitgene, they found that the sperms contained RNA,
as well as DNA. The researchers then injected this RNA into fertilized eggs of normal mice,
which do not carry the Kittm1Alf gene, and found that the treated eggs developed into mice with spotted tails.

Controlled expression of cardiac-directed adenylylcyclase type VI provides
increased contractile function; Gao MH, Bayat H, Roth DM, Yao Zhou J, Drumm J,
Burhan J, Hammond HK; Cardiovascular Research; Volume 56(2); 197-204; November

Description: This article falls under the field of cardiology research,
specifically heart failure, which is the number one cause of death in the
United States. It deals with the controlled expression of adenylylcyclase type
VI (AC6) in the heart, which provides increased contractility in response to
heart failure. AC6 is an enzyme in the beta-adrenergic receptor signaling
pathway which catalyzes the formation of cAMP from ATP. Increased cAMP
production is known to increase heart contractility.

Controlled expression refers to the ability to activate or deactivate a gene.
The main question posed by this paper is whether or not AC6 can or can not be
regulated in cardic-specific expression while still increasing heart function.
This article proposes the use of tetracycline as the regulator for
cardiac-specific expression of AC6. Regulation is of central importance to
these studies because in the case that AC6 expression leads to negative
outcomes in a patient, one would need the ability to deactivate the gene.

This paper would be a useful and interesting learning tool for the class,
because it addresses the practical application of genetics for medical
research. More specifically, it discusses gene transfer techniques, the use of
transgenic mice as model systems, regulated gene expression, and the use of
polymerase chain reaction (PCR). All of these topics are important to the field
of genetics and are applicable to our class, and this article is a good display
of how several genetic techniques can be combined to address medical ailments.

Molecular origins of rapid and continuous morphological evolution, Fondon, John W. III, and Garner, Harold R., PNAS, vol. 101, 18058-18063, December 28, 2004
"Genetics, development and evolution of adaptive pigmentation in vertebrates", H E Hoekstra, Heredity (2006), Vol. 97, 222–234, Published online 5 July 2006
This article addresses the following questions: 1) Are adaptive changes predominantly caused by mutations in regulatory regions or coding regions? 2) is adaptation driven by the fixation of dominant mutations? and 3) to what extent are parallel phenotypic changes caused by similar genetic changes?

I feel as though this would make for an interesting class because pigmentation is such a visual topic. Plus the main issues don't seem to be too far beyond the scope of the class, i.e. not too overly complex issues. In addition, it allows up to study both the genotype and the phenotype with relative ease due to the extreme visual nature of pigmentation.

“The Contributions of Sex, Genotype and Age to Transcriptional Variance in
Drosophila Melanogaster”, Gibson, Greg, Wei Jin, Gisele Passador-Gurgel,Rebecca
M. Riley, Russell D. Wolfinger, Kevin P. White, Nature Genetics, 29, 389-395,

In this research article, researchers examine the magnitude of gene effects of
various components. Contributions of sex, genotype and age to transcriptional
variance in Drosophila melanogaster are researched carefully in this
experiment. The question of whether sex, genotype, or age affect transcription
and therefore the pheneotype is being raised in this article. And if any of
these various components do, by what quantity, or to what degree are effects
observed. This interpretation is compromised to some extent by issues relating
to power and experimental design.
This article explores the many other possible factors thay may contribute to
gene expression. The study introduces to us how your phenotype maybe affected
by numerous and various factors. Furthermore, this article shows importance of
experimental design. How we must be careful to what type of experiment we set
up, so we can get the best fit data for results.

Molecular Genetics of Parkinson’s Disease, M.I. Shadrina and P.A. Slominsky,
RUSSIAN JOURNAL OF GENETICS, Vol. 42, No.8, pp. 858-871, August 2006

The article reviews the significant advances that have been made in studying
genetic factors underlying Parkinson’s disease. It fist talks about the
monogenic (familial) form of the disease and describes the novel genes that
have been discovered, whose mutations and polymorphisms lead to the
parkinsonism development (particularly the parkin and dardarin genes). The
article then talks about the more frequent, sporadic form of the disease and
describes the potential candidate genes for this sporadic form that have been
discovered. The article then mentions that the number of studies that have been
carried out for most of the candidate genes is too small to conclusively
evaluate the individual contributions of the genes to the parkinsonism
development. The question that the article poses is: what is the genetic basis
of the more frequent, sporadic form of Parkinson’s disease? (is the sporadic
form of the disease caused by mutations and polymorphisms of the same genes as
the monogenic form of the disease or is it caused by mutations and
polymorphisms of the candidate genes or a combination of the two?). The article
proposes a way to answer this question (by conducting a thorough analysis of
the genes related to the monogenic form of Parkinson’s disease in patients with
sporadic and familial parkinsonism and by carrying out associative studies of
the candidate genes of the sporadic disease form). The article concludes by
pointing out that if this question is answered, it will become much easier for
other questions to be answered. These questions include: what are genetic
markers of the high risk for Parkinson’s disease?, what is the molecular basis
of the pathogenesis of Parkinson’s disease?, and what are possible methods of
preclinical diagnostics and pathogenic therapy on this basis?
I chose this article because I think that it would make for a very
interesting class. This is because Parkinson’s disease is an important problem
in the society in which we live. In most world populations, at least 2-4% of
persons older than 65 and at least 1% of persons older than 50 years of age
suffer from Parkinson’s disease. This may not seem like a lot, but it actually
is when you consider that there are over 6 billion people on Earth. And in
recent years, the amount of people with Parkinson’s disease has increased and
the age of onset of Parkinson’s disease has decreased. So Parkinson’s disease
is definitely a huge problem around the world. I think that it would be
beneficial for students to understand the genetics behind this disease and what
causes this disease. I believe it is much more interesting to learn about things
that actually affect people around the world (such as the genetics behind
diseases) than things that have no effect on people. And I believe that the
genetics behind Parkinson’s disease is particularly interesting and certainly
worth learning about. Therefore, I think that the article that I chose would
make for a very interesting class.

Worsening of obsessive–compulsive symptoms under methadone

Yasser Khazaal, a, Sonia Krenza, Messaoud Benmebareka and
Daniele Fabio Zullinoa

Progress in Neuro-Psychopharmacology and Biological
Psychiatry, Volume 30, Issue 7, 30 September 2006, Pages

The article is interesting because OCD is a disorder that
many people are familiar with and it is common belief that
people have a genetic disposition for rituals or control
issues. However, now with the idea that opioids can lead
to OCD tendencies in seemingly "normal" people can help
explain other disorders brought about due to drug intake.
This article contains no figures so it will not be visually
compelling, but it does have a case study and I think could
lead to broader discussions of drug use and the
temporary/permanent neural alterations that can occur as a

The Use of Racial, Ethnic, and Ancestral Categories in Human Genetics Research,
Race, The Race, Ethnicity, and Genetics Working Group, American Journal of
Human Genetics, Volume 77, pgs. 519-532, August 29, 2005

Within this article titled “The Use of Racial, Ethnic, and Ancestral
Categories in Human Genetics Research,” many questions arise about the use of
racial, ethnic, and ancestral categories in genetics research and how do we
categorize people based on genetic factors. The main question that is put
forward in this article is the question of whether the use of racial, ethnic
and ancestral categories even belongs in human genetic research. Many believe
that the use of these categories can justify and even perpetuate racial and
ethnic discrimination. Some who favor the use of these categories believe that
using race, ethnic, and ancestral history can actually dispel stereotypes by
showing how biologically close we are to one another. . The evidence that
there are health disparities within each categorical group suggests that there
is a need for these categories, but many would prefer to be liberated from
these categories because of the stereotypes and the discrimination received
from these categories.
Another question that is raised within this research article is how one
distinguishes racial, ethnic, or ancestral groups from the other. The problem
with finding the answer to this question is that it is very hard to categorize
groups because of the diverse backgrounds of individuals and the complex
outlines that are needed to differentiate the human population. Also, many of
the 6.5 billion people in the world do not know about their ancestral
background or claim to be in another category than their biological evidence
would prove. These are only a couple of the many arguments that are displayed
throughout this detailed article. A racial, ethnic, and ancestral grouping is
just one argument of the many in genetic research that will only be solved by
This article would make for an interesting class because of the great
diversity that is displayed within our classroom alone. According to the
University of Texas at Austin Office of Institutional Research Office, only
57.4 percent of the fall 2005 student body claimed to be white. Meaning that
over 40 percent of the student body is of some other ethnic race. I believe
that this article will be interesting to all races because of the racial and
ethnic stereotypes that are placed among the students everyday. Racial and
ethnic backgrounds play important roles of each individual in the classroom and
it would be interesting for the students to relate their genetics class to their
lives. The classroom should be a place where we become more knowledgeable about
what is going on in the outside world and this article can stimulate one’s
desire to research and find out more about human genetics research and the
effect it plays on racial and ethnic discrimination. The article states that
“as the complex origins of human traits, behaviors, and diseases slowly are
unraveled, how genetics research is conducted could influence whether racial
and ethnic discrimination increases or decreases over time.” I also believe
that if the question of whether or not racial, ethnic, or ancestral categories
be used in human genetic research be raised in the classroom; there would be a
great discussion or even a debate over this topic.
Other interesting topics are also found in this article. Including a short
history of the first anatomically evolved human and its origin, how humans are
genetically less diverse than one another compared to other mammals, and the
reason for some physical differences within each group.

A study of identical twins’ palmprints for personal verification, Adams Wai-Kin
Kong, David Zhang, and Guangming Lu, Pattern Recognition, Volume 39 Issue 11,
Pages 2149-2156, 11 April 2006.

This article is about a study made on biometrics and identical twins. Many
identification problems arise with the inability to distinguish biometrics in
identical twins. Twins are not easily distinguishable in court, twins can use
their gift in crimes like fraudulent insurance compensation, and twins can
easily sneak in and out of places pretending to be one another. All these
problems need to be solved with more sophisticated technology for biometrics.
The study examined palmprints from the same DNA to uncover genetically related
palmprint features. The conclusion was that palmprints contain genetically
related features as well as genetically unrelated ones that can be used for
classifying identical twins.

I have a special interest in this kind of study because I myself am an identical
twin. My sister and I recently participated in a similar study currently being
conducted in the UT psychology laboratory and are eager to find the results
from that study. Identical twins are mind-boggling in that they provide an
excellent opportunity for researching the nurture vs. nature debate that has
been going on forever. What makes us who we are, genetics or the environment?
This study provides new research in distinguishing twins, which is very

Article Title: Mother knows best: Epigenetic inheritance, maternal effects, and
the evolution of human intelligence
Author: David F. Bjorklund
Journal Title: Developmental Review
Volume: 26, Issue 2
Page Numbers: 213-242
Date of Publication: June 2006

There are numerous theories in the nature vs. nurture debate, but according to
this researcher, nature and nurture interact with one another to determine
characteristics. Genes are influenced by the environment, especially during
early development. Some genes need a certain type of environment in order to
be expressed. Thus, in different environments there are different
characteristics, and depending on the environment, certain characteristics will
prevail and evolve over time. These genes include those that express
phenotypes, behavior, and intelligence. One correlation discussed in
particular is how human intelligence is affected by mothering (chimps raised by
humans show cognitive ability that is more human-like as opposed to wild

This raises numerous questions that may not get as much attention as deserved.
How much depends on the environment in natural selection in the evolution of
mankind, as opposed to the ability of a person’s genes to adapt and change in
certain environments? With this outlook on development, natural selection
becomes a matter of the “survival of the fittest genes”. Also, how do parents
deal with knowing their child has a certain “bad” gene that has a possibility
of being expressed? These genes could include a possibility for homosexuality
or even psychological disorders such as depression. Do parents set up an
environment that discourages “bad” genes from developing, and will that tactic
actually work? Lastly, to what degree do certain characteristics owe their
evolutionary change to the environment? It seems as though some
characteristics, such as phenotypes, are affected more by the environment than
others, such as intelligence, and will evolve more quickly.

Different people have different opinions on how the environment affects the
development of a person and how a person becomes who they are. In the past,
the environment was never given much credit for this development, and genes
were given the most attention. But now, as more research is done, new light is
being shed on the role of the environment. I find the topic very intriguing
since it deals with how people develop into themselves and how characteristics
of species, and thus the species themselves, have evolved over time due to
factors beyond their control (the environment). Although we've already
somewhat discussed this topic in class, I feel that it deserves more attention
- it would be interesting to hear the different opinions of classmates on this
seemingly controversial topic.

Genetic and Environmental Influences on Eating Behavior: The Swedish Young Male Twins Study,   Sanna Tholin, Finna Rasmussen, Per Tynelius, and Jan Karlsson,   The American Journal of Clinical Nutrition,   Vol. 81 No.3,   p. 564-569,   March 2005
The article unravels the question of whether eating habits is influenced mostly by genetics or environment by studying twins of a certain population, Swedish young male twins. The dimensions of eating behaviors studied and questioned are cognitive restraint, emotional eating, and uncontrolled eating.
GENETICS: The Critical Region in Trisomy 21, David L. Nelson and Richard A.
Gibbs, Science, Vol. 306, pp. 619-621, October 2004.

This article discusses the question of whether triplication of the 33
critical-region genes is directly responsible for the craniofacial
abnormalities of Down Syndrome. The authors discuss a mouse model used to
figure out whether or not this is true. I think that discussion of this article
will make for an interesting class because Down Syndrome is one of the most
common genetic diseases, and affects 1 out of every 700 children. Therefore,
many of your students probably know people who have been affected by this
disease, and would be interested in hearing about this.

Genetics of Osteoporosis
Huang, Qing-Yang and Annie Wai Chee Kung
Molecular Genetics and Metabolism, volume 88, pg. 295-306, August 2006

Osteoporosis is basically a bone disease that causes the bones of individuals
to become brittle over time ans thus leading to the cumulative fracture of the
bone itself. This disease has been noticed at a higher ratio if women in
compared to men, especially in post-menopausal women and those over 80.
Osteoporosis is caused by lower and lower Bone Mineral Density, or BMD, in
which causes the bone to lose bone density and strength over time which
scientists believe to be affected both by the genetics make-up of the
individual as well as the environment that they are placed in.
The two researchers from the University of Hong Kong that posed a question of
how much of the effects of osteoporosis is based on the genetic material of
each individual. Overall, the researchers were taking a deeper look on the
connection of certain genes and linked genes as well to the cumulative effects
that they cause on the degenerative bone disease. The two researchers decided
to use both mice and human genome to identify the specific genes that cause
this disease and if there is substantial connection between these genes to the
severity it affects the disease. The basic concept behind their research was
to find any sort of connection between the genetic makeup of an individual and
the expression of the disease. The research later produced the result that the
human gene ALOX12 was a significant contributor to BMD degradation. They also
discovered that certain loci locations on sex-linked genes and in polymorphism
also account on why women suffer more severely from osteoporosis than men which
provided proof to the original hypothesis.
I believe that this article is relevant to the current topics that we are
currently covering in class in that it deals directly to how genetics affect
the pathogenesis of osteoporosis. The article covers how certain genes
directly affect the individual and whether or not they will suffer osteoporosis
later on in life. This is another example to the idea of whether or not
genetics affect either the personality and physical status of people such as in
homosexuality to diseases such as cancer. It asks the question of whether genes
or the environment has more effect on osteoporosis or maybe caused by a factor
or both in equal say. Therefore, the researchers performed an experiment in
which they mapped out certain suspicious genes and that they suspected to cause
the disease in mice and humans and then compared the results. This experiment
was actually performed very thoroughly using strong inference in that they knew
exactly which genes to look at for both species and even carried out gene
mapping cases between males and females as well as in twins. After all the
experiment and mapping of genes the researchers realized that it was indeed
certain regular and sex-linked genes that account for low BMD ratios in certain
individuals. With clean experiments and certain results they decided that women
were more susceptible to osteoporosis, there was a higher chance in twins to
both get osteoporosis if one had certain genes, and that the disease is much
more dependent on genetics makeup than the environment in that the disease is
also dependent on foods consumed and activities of the individual. I believe
that this article will prove to be very interesting for the class in that it is
a modern day and pretty recent research experiment that was performed using
concepts of strong inference directly involving the major concepts of genetics
in studying certain genes that cause diseases in people. It is basically a
real life example of all the points that we have covered in the class.

“Single nucleotide polymorphisms in DNA repair genes and basal cell carcinoma of

Ranjit Kumar Thirumaran, Justo Lorenzo Bermejo, Peter Rudnai, Eugene Gurzau,
Kvetoslava Koppova, Walter Goessler, Marie Vahter, Giovanni S. Leonardi,
Felicity Clemens, Tony Fletcher, Kari Hemminki and Rajiv Kumar

Carcinogenesis, vol.27, pp.1676-1681, February 25, 2006

Every year thousands of Americans are affected by various skin cancers, and the
most common form of skin cancer is known as basal cell carcinoma or BCC.
People generally correlate skin cancer with excessive exposure to UV radiation,
but that is not the only factor that influences the individual susceptibility to
BCC. Genetic factors also play important roles. Functional repair enzymes are
needed to remove the photoproduct formed by UV exposure in the DNA of skin
cells, and to repair the broken strands that consequently occur. Individuals’
susceptibility to skin cancers, including BCC, varies directly with the repair
capacity of their DNA. In this article, the researchers specifically want to
determine the risk modulation of BCC by variant allele for T241M polymorphism
in XRCC3 gene and gender specific effect by E185Q polymorphism in NBS1 gene.

I think this article would make an interesting topic for the class because it
presences another case between the debate of nature and nurture. Many people
believe that skin cancer is strictly caused by environmental factors, such as
exposure of UV radiation. However, the result of this research indicates
otherwise. The results of the study do not show a statistically significant
correlation between the amount of sun exposure and risk of BCC. On the
contrary, they show that carriers of variant T-allele for T241M polymorphism in
XRCC3 gene have a statistically significant decreased risk of BCC. Also, I
thought it would be interesting for the class to see that the risk of BCC is
different in each gender due to the variant allele in a gene.

Neuromedin ß: a strong candidate gene linking eating behaviors and
susceptibility to obesity

Luigi Bouchard, Vicky Drapeau, Véronique Provencher, Simone Lemieux, Yvon
Chagnon, Treva Rice, DC Rao, Marie-Claude Vohl, Angelo Tremblay, Claude
Bouchard and Louis Pérusse

The American Journal of Clinical Nutrition
Vol. 80, No. 6
Pp 1478- 1486
September 2, 2004

The obesity epidemic has become one of the most important public health problems
of our generation. During the past 20 years, there has been a dramatic increase
in obesity in the United States. The recent increases in the prevalence of
overweight and obesity are reflected across all ages, racial and ethnic groups,
and education levels in the U.S. Despite recent advancements in our
understanding of obesity, our capacity to prevent weight gain and to treat
obesity is still far from adequate. Obesity is frequently associated with
eating disorders, and evidence indicates that both factors are influenced by
genetic factors. Although several genes have been shown to be associated with
obesity, little is known about the genes influencing eating behaviors in
humans, despite evidence that abnormal eating behaviors and disorders are
frequently encountered in obese subjects. I feel like the objective of this
experiment, to identify genes associated with eating behaviors, would be
interesting and beneficial to study because it provides information that
directly affects our life and well being in multiple ways.

A relation between eating behaviors and obesity has been suggested in multiple
studies, but there is also evidence that these behaviors are governed by
genetic factors. Persons who binge eat or who have bulimia nervosa or anorexia
nervosa are also characterized by dysfunctional levels of cognitive dietary
restraint, disinhibition, and susceptibility to hunger compared with normal
subjects, and they also have an important heritability component. Despite
the fact that eating behaviors are partly heritable traits, little is known
about the genes influencing them.

The Quebec- Family Study is designed to investigate the genetics of obesity.
Three eating behavioral traits, cognitive dietary restraint, disinhibition, and
susceptibility to hunger were assessed with the use of the Three-Factor Eating
Questionnaire. In the Québec Family Study (QFS), disinhibition and
susceptibility to hunger were positively associated with BMI, body fatness, and
waist circumference. To confirm or provide new quantitative trait linkage
analyses, to identify the genes influencing the eating behaviors, and to
provide new chromosomal regions, a genome-wide scan linkage analysis was
undertaken in the Quebec Family Study. Taking into account body composition
and macronutrient and energy intakes, a genome-wide scan was conducted with
genetic markers spanning the 22 autosomes to identify quantitative trait loci
for eating behaviors. Two approaches were used to test for linkage between
eating behaviors and the genetic markers. Linkage was tested with the
Haseman-Elston regression-based sibpair linkage procedure as well as with the
variance components based approach. Genome-wide linkage analyses provide an
opportunity to identify chromosomal regions that harbor genes influencing
complex traits, such as eating behaviors. Using this approach, four
quantitative trait loci were identified for disinhibition and susceptibility to
hunger while no evidence for linkage was found for cognitive dietary restraint.
Genetic associations were assessed by analysis of covariance comparing mean
phenotypic values across Neuromedin Beta genotypes. The results of this
experiment suggest that Neuromedin Beta is a very strong candidate gene of both
eating behaviors and predisposition to obesity.

Association of GABRA2 with Drug Dependence in the Collaborative Study of the Genetics of Alcoholism Sample

Behavior Genetics: Volume 36, Number 5/September 2006. Pgs 640-650.

Arpana Agrawal, Howard J. Edenberg, Tatiana Foroud, Laura J. Bierut, Gerald
Dunne, Anthony L. Hinrichs, John I. Nurnberger, Raymond Crowe, Samuel Kuperman,
Marc A. Schuckit, Henri Begleiter, Bernice Porjesz and Danielle M. Dick

This study focuses on a series of twin studies that found certain genetic
factors to be influential on alcohol and illicit drug dependence. It explores
the relationship between GABRA2 and illicit drug dependence in the
Collaborative Study on the Genetics of Alcoholism with two goals in mind. Genes
in the GABAA receptor gene cluster on the 4p3-12 are to be examined in order to
determine whether they are associated with marijuana and other illicit drug
dependence. In addition, the extent to which the association between these
genes and alcohol dependence varied according to the individuals with
co-occurring drug dependence will be examined.
In 2003, approximately 20 million Americans ages 12 + were illicit drug users.
Family studies have shown that drug disorders cluster in families and that
relatives of individuals with drug problems are at a higher risk of having drug
problems themselves. This is an important topic that relates to several
individuals our age. Not only is it interesting, but this article also relates
to what we our learning in class in relation to nurture vs. nature.

"Isolation of a human gene that inhibits HIV-1 infection and is suppressed by
the viral Vif protein"; Ann M. Sheehy, Nathan C. Gaddis, Jonathan D. Choi and
Michael H. Malim; Nature 418, 646-650 (8 August 2002)

Many viruses develop ways to overcome host-mediated mechanisms that prevent the
viruses from being infectious. HIV-1 is a virus that codes for a protein called
Vif (virion infectivity factor) and this protein is necessary for it to
replicate and infect other cells. Human T lymphocytes have an innate antiviral
phenotype (via gene, CEM15) which is inactivated by this Vif protein. The
question then arises that if the production of Vif protein is interrupted,
could the CEM15 antiviral phenotype help fight the infection?

This article is interesting in that it investigates the DNA's innate ability to
fight off viral infections and how HIV is able to overcome these natural
defenses by producing a specific protein. Being a regulatory circuit, it also
reinforces the idea of the protein inhibition of genes, i.e. gene expression.
Also this research could spawn discussion over other viruses and whether they
behave in a similar way.

Fluctuating asymmetry in certain morphological traits in laboratory populations
of Drosophila ananassae
Vishalakshi C, Singh BN
GENOME 49 (7): 777-785 JUL 2006

In this article, the authors were mainly interested in finding out about
fluctuating asymmetry in Drosophila ananassae. Is it caused by genetic or
environmental factors? Are they more frequent in certain populations? Are
females more prone to fluctuating asymmetry than others? They also focused on
fluctuating asymmetry in five certain traits to see in which populations or
which sex they were more frequent. This would make for an interesting lecture
because it discusses nature vs. nurture while also exploring the differences
between the sexes and their susceptability to genetic influences and
environmental factors.

Three allele combinations associated with Multiple Sclerosis, Olga O Favorova 1,2, Alexander V Favorov 3, Alexey N Boiko 4, Timofey V Andreewski 2, Marina A Sudomoina 1,2, Alexey D Alekseenkov 2, Olga G Kulakova 1, Eugenyi I Gusev 4, Giovanni Parmigiani 5 and Michael F Ochs 6, BioMed Central Medical Genetics 2006, Volume 7, 1-9* (Online Article, no page numbers given), 26 July 2006.
       This article can be best described as one that does not pose a question, but rather one that discusses the complexity genes in our body.  This article discusses the illness is MS or Multiple Sclerosis and how it can be in ones genes to get this illness at some point in their life.  The difficulty in identifying whether or not the disease is genetic in yourself is due to the fact that there are so many gene combinations that could be causes for the disease.  We do not know whether it is one group of genes or many different groups of genes that make up whether or not someone can get MS.  This particular article discovers 2 new combinations that can be the cause of someone getting MS through their gene pool.  In class we have brushed upon the idea that alleles are alternative forms of certain genes, and this article gives a real world example of how dominant and recessive genes work.  This article also would be interesting in class because it gives students who are Pre-med, or Pre-health in general a glimpse into the kinds of scientific literature they will have to read and learn about in order to become the future doctors, researchers, dentists, pharmacists, etc of the future.  It also is a good article for people who are studying biology to become scientists, because you get a chance to learn about genetics and how it applies to humans, as well as getting a better understanding of how genetics works in terms of our health.  This article is also interesting because it helps to see how genes work in the human body in general, it would help to understand why it is that our hair colors or our eye colors are what they are.

“Genetics: A Genomic View of Animal Behavior,” Elizabeth Pennisi, Science, Vol.
307, pages 30-32, January 7, 2005.

This article asks many questions concerning the link between genetics and
animal behavior. Though animal behavior is already studied by evolutionists
and other biologists, what role does genetics play? Is a certain animal
behavior stimulated by a cue from their environment, a complex interaction
between genes, or both? Also, how does a particular gene operate in several
different species—does it influence generally the same behavior or something
completely different? What other behaviors does one gene influence? How many
genes influence one behavior? These last three questions were pivotal in
several experiments the article discussed, which include: how an unidentified
gene (dubbed forager, which codes for a protein called cGMP-dependent protein
kinase (PKG)) controlled how much a fruit fly wandered and how readily they
responded to sugar, and also how the same gene proved key to feeding behavior
in other invertebrates as well; how researches used microarrays to look at the
differences that distinguish bees that tended the hives from bees that left the
hive for pollen, and found 2200 out of 5500 genes examined whose brain activity
varied between the two different bees; and how if any component in the
“micronetwork” that causes a mouse to be able to recognize other mice it is
familiar with is removed, then the mouse loses its ability to tell a familiar
mouse from a stranger. Many other experiments were discussed in the article,
including the genetic basis for the presence of studs and social outcasts among
male chichlids. Another question posed in the article was if the way genes were
regulated was just as important as the proteins they produced, in the instance
of the prairie vole, which is faithful to its mate, and meadow voles, which are
not. Larry Young of Emory University found that a regulatory region was longer
in the monogamous species, and when he put the prairie vole’s vasopressin (the
neuropeptide governing this trait) receptor gene and its regulatory region in
mouse embryos and meadow voles, both became more faithful than typical.
Lastly, Michael Meaney from McGill University found that a different regulatory
region, called a promoter, is pivotal in the social relationship between parents
and their offspring, and demonstrated that when a mother rat fails to lick and
groom her newborn pups, chemical changes in DNA bases make those pups grow up
timid and abnormally sensitive to stress.
As an Evolution, Ecology and Behavior major, I find this article very
interesting and useful, especially since it tries to link genetics to several
other areas of Biology. As said in the article: “ ‘There is this clear gulf
between people who are using modern genetic techniques to study very specific
questions and the people who are studying natural diversity,’ adds Steve Phelps
from the University of Florida, Gainesville. But as more behavioral scientists
take up the tools of genomics and comparative biology, the payoff may be a
deeper understanding of the molecular basis of behavior in animals--even
people--and how behaviors originally evolved. The field ‘is very ripe for a
productive synthesis,’ says Phelps.” This article is a great example of how
genetics can solve certain mysteries other areas of Biology are having, and how
“crosstalk between disciples” can help clear up some of these mysteries.

Title: Genetically modified crops: success, safety, assessment, and public
Authors: Om V. Singh, Shivani Ghai, Debarati Paul, and Rakesh K Jain
Journal: Applied Microbiology and Biotechnology Vol 71 August 2006

This article explains what is done to make genetically modified crops. It
describes the different ways they can insert transgenes derived from other
plants or organisms into the crops DNA to change some characteristic of the
crop. This process is becoming more popular and has been widely used in recent
history but there is still ethical/social dilema. People are concerned about
what this does to the plants that ultimately end up eaten by humans and what it
does to the environment. The article lists some of the great positive results of
genetically modified crops and also the areas in which there is a risk to people
or the environment. This is a good article because it deals alot with the
social context and how this technology is regulated by public concern. The
people are afraid and want to know what is in their food. This technique could
make even greater advances than are already in place but more research is
needed to ensure safety to the consumer.

Genetic Covariance Among Measures of Information Processing Speed, Working Memory, and IQ

M. Luciano, Behavior Genetics, Volume 31, pgs 581-592, November 2004

This article describes a study which aims to settle the heated debate between nature and nurture's role in intelligence.  Is intelligence a gift handed down from parents or is it something earned through lifetime experiences?  If intelligence is indeed genetic, then where in our DNA is it coded?  With this exciting research, along with many recent advancements in genetic engineering, perhaps a more intelligent human race can be created.  Furthermore, if intelligence is not derived from our genes, what creates the variation in intelligence?  More research can be done on shaping the young minds of children into more intelligent adults.  The study performs extensive tests on sets of identical twins.  The measures of IQ are separated into information processing speed, working memory, and complex cognitive processes, in order to assess individual parallels between subjects.  The results of the study show strong correlation between genotype and performance on nearly all three tests.

"The use of cDNA microarray to identify differentially expressed labor-associated genes within the human myometrium during labor"
M. Sean Esplin MD et al
American Journal of Obstetrics and Gynecology
Volume 193, Issue 2 , August 2005, Pages 404-413
This article asks the question: What genes are expressed only in humans who are in labor?  In other words: Which are the labor-specific genes?
<>The researchers used cDNA microarray technology to identify those genes differentially expressed during labor, and then used multiple methods for confirmation: RT-PCR, Northern blot, and in-situ hybridization.

Effect of Limited DNA Methylation Reprogramming in the Normal Sheep Embryo on Somatic Cell Nuclear Transfer, Nathalie Beaujean, BioOne, pp. 185-193, Published March 1, 2004

The demethylation of cytosine in the sperm genome before a functional zygote is formed is thought to be an important function of the oocyte cytoplasm for subsequent embryonic development in the mouse. This event does not occur in the sheep or rabbit zygote and occurs only partially in the cow. The aim of the study was to investigate the effect of limited methylation in the normal sheep embryo. Sheep fibroblast somatic nuclei were only partially demethylated and underwent a stepwise passive loss of DNA methylation during early stages. Our results suggest that somatic nuclei that do not undergo rapid reorganization of their DNA before the first mitosis fails to develop within two to three cell cycles. However, because only embryos with certain chromatin appear to survive the morula stages, failure to demethylate the cells of the blastocyst is likely to directly impact on developmental potential by altering programmed patterns of gene expression. Thus, remodeling of DNA appears critical for development of both fertilized and nuclear transfer embryos.

I think this would be a great article for our class because we spoke about methylation being an indication for the expression of certain proteins. In this case demethylation is occuring for growth and developmental reasons.

Genetic Influences on Female Infidelity and Number of Sexual Partners in Humans: A linkage and Association Study of the Role of the Vasopressin Receptor Gene (AVPR1A)
Lynn F. Cherkas, Elizabeth C. Oelsner, Y.T. Mak, Anna Valdes, and Tim D. Spector
Twin Research
Volume 7 Number 6
pp. 649-658
December 2004
This article examines a research study where 1600 randomly-selected female twin pairs from the United Kingdom confidentially reported their experience with unfaithfulness, their attitudes towards their infidelity, and their total number of sexual partners. The purpose of the study was to determine if infidelity and sexual promiscuity are heritable or affected by environmental influences, and if they are associated with the vasopressin receptor gene, a locus implicated in other mammal’s sexual behavior. The results showed that variation in infidelity and in the number of sexual partners can be explained by genetic variation with little or no role for environmental factors, and that they do have a heritable component. For example, identical twins are approximately one and one-half times more likely to be unfaithful, if their twin is unfaithful. However, attitudes towards infidelity were explained mostly by environmental influences. Also, the analysis did not support the hypothesis that the vasopressin receptor gene could explain variation in human sexual behavior. In addition, the article talks about how this supports evolutionary theory that promiscuous sexual behavior is advantageous for women and is part of a selective evolutionary process.
I believe this article will be interesting for class discussions because it addresses the correlation between psychological behavior and genetic influences. Most of us consider sexual promiscuity to be an environmental factor; however, this study forces us to reexamine our preconceptions.

Can random mutation mimic design? A guided inquiry laboratory for undergraduate
students, Steven T Kalinowski, Mark L Taper, and Anneke M Metz, Genetics 2006;
Volume 173, Issue 4, August 2006, published ahead of print on September 1, 2006

The main goal of this paper is to explore the question and simulate a possible
answer of whether random mutation can create complex biological structures that
appear designed by using paper airplanes as the model organism. Some structures
in living organisms seem so complex and therefore have been said to be evidence
of intelligent design. The purpose of the guided lab is to investigate
evolution by using a paper airplane and also to invoke scientific thinking.

I think this would be a good article for the class because it is brings into
play many difficult ideas and questions about human evolution and the ability
of random mutation yet creates a more simple method for answering them. The
paper airplanes serve as a great model organism because the “fitness” of each
plane, shown by the distance it flies, is a task of its ability to mutate
independently. Those that are built best (by random changes made in its
structure) fly farthest, and those that fly farthest model those that are able
to reproduce sucessfuly by selection. The guided lab is useful in teaching
students for themselves how natural selection works is a good introduction to
understanding how complex adaptations can evolve.

Appetite Control, Katie Wynn, Sarah Stanley, Barbara McGowan, and Steve Bloom,
Journal of Endocrinology, Vol. 184, 291-318, 2005.

In the last decade our body weight and food intake has increased immensely
as well as our understanding of the physiological systems. Our bodies transfer
different signals via neuropeptides which regulate energy homeostasis. For
example, insulin and hormones have a great effect on influencing our body
circuits. This review discusses central neuronal networks and different
signals which contribute energy homeostasis, and how a loss of the homeostatic
process may result in obesity. However, it has been argued that evolutionary
pressure has resulted in a drive to eat with out limit when food is readily

Our bodies must continually balance food intake with energy expenditure.
Many hormones initiate and terminate a meal. I think that this article is
extremely interesting because Americans are overweight and it is partially due
to the way they treat themselves on the inside and the outside. A proper
nutrition starts on the inside of the body with knowledge of ones own hormones
and how energy homeostasis takes place. When an individual understands how his
or her own body works then they might think different about what they put into
their bodies.

I am also very interested in diet and appetite control because as a woman
at The University of Texas I have witnessed first hand how other women have an
appetite that is out of control, or on the other hand no appetite at all. I
think if we could reach out to them with something that may make them
reconsider the lettuce they eat three times a day, or the triple cheeseburger
that they eat at three in the morning, women may have a better understanding of

Genetic mapping of a 17q chromosomal region linked to obesity phenotypes in the
IRAS family study, BS Sutton, CD Langefeld, JK Campbell, SM Haffner, JM Norris,
AL Scherzinger, LE Wagenknecht, DW Bowden, International Journal of Obesity, 30,
1434-1441, 7 March 2006

Obesity is a complex disorder that affects a significant percentage of the US
population. “Although the environmental changes in the industrial world (i.e.
food intake, sedentary lifestyles, etc) are often blamed for the overall
increase in this epidemic, an individual’s genetic susceptibility is also a
major contributory factor” (BS Sutton et al, 1434). In this article, a
research conducted explores DNA samples of a group and the regions on their
genomes that contribute to an unknown “obesity gene.” “A major aim of the IRAS
Family Study is to identify chromosomal regions and specific candidate genes
associated with obesity-related traits in two ethnically diverse cohorts:
Hispanic and African Amerian” (1434). Information taken from the subjects that
underwent the study include six primary obesity phenotypes, including BMI, waist
circumference, waist-hip ratio, VAT, SAT, and visceral –subcutaneous ratio.
Blood samples taken from the subjects were then analyzed. Through genomic
mapping, chromosome 17q was linked to three of the obesity phenotypes thus
relating a specific chromosome to the “obesity gene.”
I think this article would be interesting for class because so much can be
speculated about the different causes of obesity. This article provides an
alternative and proven answer to the cause of obesity through genetics. Since
the results show that obesity is linked to a specific chromosome, thought
provoking explanations can be speculated on different approaches of treating

Article Title: Gene therapy that inhibits NF-.B results in apoptosis of
human hepatocarcinoma by recombinant adenovirus
Authors' names: Tie-Jun Li, Li-Ping Jia, Xiao-Ling Gao, Ai-Long Huang
Journal Title: World Journal of Gastroenterology ISSN 1007-9327
Volume: 12
Page Numbers: 5287-5292
Date of Publication: September, 7, 2006
The question being asked here is whether or not the recombinant adenovirus
induces the TNF-a-mediated apoptosis in vivo. The reason why I believe it will be interesting for the class is because it applies genetics into researching whether or not genetic material is capable of helping us create a potential treatment for liver cancer. This article is well organized and detailed enough to help us understand what they have done.

Genetics of cattails in radioactively contaminated areas around Chornobyl., Tsyusko, O., Smith, M., Oleksyk, T., Goryanaya, J., & Glenn, T., Molecular Ecology, Vol. 15 (9), pp. 2611 - 2625, August 2006.
Article Title: Restriction of vaccinia virus replication by a ced-3 and ced-4-dependent pathway in Caenorhabditis elegans
Authors NamesWan-Hsin Liu,Yi-Ling Lin, Jia-Pey Wang, Willisa Liou, Roger F. Hou, Yi-Chun Wu, and Ching-Len Liao
Journal Title: Proc Natl Acad Sci U S A
Volume: 103
Page Numbers: 4174–4179
Date of Publication: Online 2006 March 6
I find these article extremely interesting because these C.elegans are almost completely resistant to viral attack. The C. elegans can however be susceptible to bacterial infections, yet viruses seem to do nothing to them. There is a huge evolutionary gap between the C.elegans and the mammals of course, but it is interesting since 19,000 of the C.elegans proteins have matches in humans, which is greater than 40% of their protein make-up.  In this study, the question arises wether or not C.elegans can be further extended as an artificial host for animal virus infections.
How could the machinery of the the C.elegans be responsible for not allowed viral infections? They scientist turned  to something called VV, which is vaccine virus. The VV can find it’s way into the machinery of SOME C.elegans, but not all. The scientist had to ask the question of why this is.  Wild type N2 strain of C.elegans cannot be infected with the VV virus. PEG is something that can help a virus interact with a host cell and allow the virus to enter inside the cell walls.  They used multiple types of staining methods and incubation times with the PEG and the VV viruses to see if the genome of the VV virus would penetrate the host cell. They tagged the VV virus with X-Gal for signs of it inside of the host cell. What was odd is that the genome of the VV virus did invade the host cells cytoplasm(which is where it normally replicates), yet something was still prohibiting the virus from forming progeny. So now they have ruled out the possibility that there is something in the extracellular matrix that might not be allowed the virus to replicate.
There must be something in the genes of the C.elegans that is prohibiting the virus from replication. C. elegans  have PCD just like human cells have. The program cell death genes in C.elegans are ced-3,ced-4, ced-9, and egl-1.  The scientist then weakened or turned the genes off in the C. elegans and all of a sudden, a sudden rise in the population of the C.elegans  was seen. Something at the genetic level was inhibiting the forming of the viruses in the cells even though they were sitting right there in the cytoplasm.  We show here that the ced-3, ced-4, ced-9, and egl-1 genes, composing the core PCD machinery, control VV replication inside C. elegans. In addition, the effects of ced-3 or ced-4 mutations on the cell-killing activity and VV replication levels in worms appear to be closely associated..
<>This is a very brief summary of what is discussed, and I think this would be a fascinating subject to continue studying more in depth in class. This takes a look at the genetic level, a organism which can resist viral attacks! I think it goes unsaid the possibilities of the secrets of the genome of C. elegan  that is to be had. This flows with this classes material, because it looks at individual genes on the genome.

Title: HLA-B Maternal-Fetal Genotype Matching Increases Risk of Schizophrenia
Authors: Christina G. S. Palmer, Hsin-Ju Hsieh, Elaine F. Reed, Jouko Lonnqvist,
Leena Peltonen, J. Arthur Woodward, and Janet S. Sinsheimer
Journal: The American Journal of Human Genetics
Volume: 79
Pages: 710-5
Electronic publication: 8/15/06


- What are the primary risk factors and causes of schizophrenia?
- Are the causes more due to the genetics of a person or by the environmental
- Do the birth complications associated with schizophrenia originate from
genetics influences also?
- Is HLA matching a risk factor in the development of schizophrenia?


- Schizophrenia heritability appears to be more due to genetics (81%) than
environmental causes (11%).

- The environmental affects that causes schizophrenia would most likely occur
very early in life (prenatal).

- Pregnancy complications are considered to be highly involved as being risk
factors of schizophrenia. These complications may even originate from genetics

- Rh (Rhesus) incompatibility is a complication that has a strong link to

- Maternal sensitization has occurred in healthy pregnancies and may actually be
beneficial for implantation and maintenance of pregnancy. Some cases in which
there is HLA (human leukocyte antigen) similarity between the mother and fetus
have resulted in increases of the risks for fetal loss and other birth
complications and defects.

- Female offspring appear to be more vulnerable to the effects of HLA-B locus
MFG (maternal-fetal genotype) matching but this may be due to pre-eclampsia, a
condition associated with HLA-B matching. Female fetuses have a higher survival
rate than male fetuses in pre-eclampsia which is why the effects of this
condition on schizophrenia may be observed more on females.


I find this article to be very intriguing because I have always been interested
by schizophrenia and its origination. If this disorder is really caused by
one's genetics as how the article had implied, then steps may be taken toward
finding a solution to prevent the risk factors from ever occurring to the
fetus. Even if a solution may not be reached yet, just being able to forewarn a
family of the possible risks of schizophrenia for their child will help to
prepare them mentally for that possibility. I must admit that I did not
completely understand all of the experiment's statistics and resulting data and
that why I do hope that we will discuss this article in class so that you can
further explain the details of the article's findings.

Title: Genetically modified crops: success, safety assessment, and public concern
Authors: Om V. Singh, Shivani Ghai,  Debarati Paul, Rakesh K Jain
Journal Title: Appl Microbiol Biotechnol
Volume: 71
Published: 26 April 2006

This article raises several questions regarding the advantages and dangers of using genetic engineering in the agricultural industry. One such advantage discussed in the article is the reduction in crop production cost, and the increase in crop yield. These advantages are due to use of genetic engineering to lead to a drop in pesticide use and an increase in the general heartiness of crops. One interesting point that the authors made was that a decrease in pesticide use, due to genetic modification, would not only reduce cost to farmers, but also reduce the amount of toxic chemicals placed into the environment.  Another question which was raised was the possibility of genetic modification leading to easy mass production of plant based biopharmaceuticals such as edible plant vaccines. The article goes on to discuss several other types of biopharmaceuticals such as monoclonal antibodies(MAbs), enzymes, blood proteins, and new types of subunit vaccines which could be mass produced safely, and at a low cost using genetic modification on crops. A final advantage which the authors raise questions about and analyze is the possibility of using genetically modified plants for environmental monitoring and remediation.  A point raised by the authors of this article regarding the dangers of using genetic modification in crops is what detrimental effects would occur on nontarget species and the environment. One such danger of using genetic engineering in the agricultural industry that this article discusses is the introduction of allergenic or harmful proteins into foods. In the article an experiment is discussed in which humans who are ileostomists were found to have modified DNA present in their digestive system from early consumed genetically modified crops. In this regard the authors raise the question if animal testing would be used to see if genetically modified crops have any toxic effects. The authors also point out that DNA from degraded plants could possibly find their way into foreign plants, giving these nontarget plants an unintended phenotype. Another danger of genetic engineering which the authors discuss is the possible loss of biodiversity. This could happen by the modified plant outgrowing the local flora. A third danger discussed by the authors is the possibility of pests developing resistance to genetically modified plants. This could occur due to the intense selection pressure on pests and pathogens populations. A final question raised by this article is that if governments around the world are doing enough to control genetic engineering in the food industry. The reason that I believe that this article would make for an interesting class is that with the growing organic industry it is necessary to discover whether or not any significant differences, regarding health and safety, exist between so called organic nonmodified produce purchased at an establishment such as whole foods market or genetically modified produce from a grocer such as HEB. Also, if so called genetic engineering is found to be safe and profitable in crops what is the next step? Genetically modifying cows so that they produce more of the desired cuts of meat? Modifying chickens so that the majority of their meat is grown in the chest? All of these situations are still yet to be proven physically possible, but in the future at what point is the line drawn when it comes to genetic engineering.

Increased glutathione S-transferase activity rescues dopaminergic neuron loss in
a Drosophila model of Parkinson's disease. Alexander J. Whitworth, Dorothy A.
Theodore, Jessica C. Greene, Helen Benes, Paul D. Wes, and Leo J. Pallanck.
Proceedings of the National Academy of Sciences of the United States of
America. v. 102, no. 22 p. 8024-8029. May 31 2005.

This article seeks to discover the mechanism by which the loss of parkin
function causes neurodegeneration. There have been identifications of genes
that cause inherited forms of Parkinson's disease. With this information they
ask what neurodegenerative mechanisms may be relevant to these forms of
Parkinson's disease. They propose that parkin is required to prevent
degeneration of a subset of DA neurons in the breain, that this degeneration is
enhanced by a loss-of-function allele of GstS1 gene and that the overexpression
of this gene prevented DA neuron degeneration in parkin mutants. With these
observations they also suggest that compounds known to induce glutathione
S-transferase expression may provide therapeutic benefits for Parkinson's

This article would make for an interesting class because this article proposes
possible mechanisms by which some forms of Parkinson's disease act and
function. Most people have had heard of Parkinson's disease and have had some
contact with it. This disease is also currently incurable. In this article it
is explained how Parkinson's affects our body as well as possible ways that
this occurs. It is also interesting because with these mechanisms it is
possible, and shown in the experiment, that the effects of Parkinson's disease
can be slowed. The work also challenges what was considered an absolute
requirement for a certain type of Parkinson's. I would think that this sort of
article would be interesting because it shows the effects of Parkinson's,
possible ways it occurs, and possible treatments for the disease.

Consistency of genetic inheritance mode and heritability patterns of triglyceride vs. high density lipoprotein cholesterol ratio in two Taiwanese family samples, Kuo-Liong Chien, Hsiu-Ching Hsu, Ta-Chen Su, Chi-Yu Yang, and Yuan-Teh Lee, BMC Genetics, volume 4, published online April 23, 2003, link: http://www.pubmedcentral.gov.content.lib.utexas.edu:2048/articlerender.fcgi?artid=155683

The question being asked is whether there's consistency in the mode of heritance and genetic components of TG/HDL-C between 2 different populations in Taiwan.  It was also questioned whether shared environmental factors would affect in controlling TG/HDL-C.  I just thought the article was interesting when there was a difference in how genetic heritability play a more significant role in TG/HDL-C within a younger community-based family than compared to older hospital-based family.  In hospital based family, shared common household effects and high spouse correlation were found significant. This implied that common household factors might play important roles in TG/HDL-C values in older age.  The study found that age-differential gene effect might be responsible for TG/HDL-C varience in different populations.  The trait can be influenced by various environmental lifestyle risk factors.  I think that we should study other factors that affect existing defects.  Its a never ending process but with each new information obtain, we can decrease the risks. 

New Insights into Migraine Pathophysiology, Sanchez-del-Rio M, Reuther U, and Moskowitz MA, Current Opinion in Neurology, volume 19, pts 294-298, June 2006

This article proposes new findings in migraine research that mainly focuses on mutations with “familial hemiplegic migraine and the role depression in its pathopsysiology and cortical spreading treatment.” The recent findings of numerous point mutations have led the authors of this article to believe that migraine may be caused by paroxysmal interruptions in the ion-translocating method. These mutations make the brain more likely to “prolonged cortical spreading depression”, which is the result of “excessive synaptic glutamate release, decreased removal of glutamate and potassium from the synaptic cleft, or persistent sodium influx”. Stopping the “cortical spreading depression” has been a point of concern as far as migraine prevention. Migraines treated with “beta-blockesrs, valproate, topiramate, methysergide or amitriptyline” lowered the “cortical spreading depressions in rats.” Studies with migraine patients also show that the appearance of cortical spreading depression as a “mechanism”. Many waves of “cortical spreading depression” in a row can also have negative effects on a patient’s brain and can cause “silent ischaemic lesions” in specific regions of the brain “such as the cerebellum”.
 So basically, there are several characteristics of migraine that show paroxysmal interruptions “in neuronal and vascular function”. This, therefore, show the disturbances in the regulation of ionic gradients. This article is interesting to me because I suffer from migraines and they also are very prominent in my family. It is something that I deal with on a weekly basis and a condition that I am currently taking medication for. 

Gene Silencing in Cancer in Association with Promoter Hypermethylation
James G Herman, M.D., and Stephen B. Baylin, M.D.
New England Journal of Medicine, Vol. 349, No. 21, pp. 2042-2054, November 20, 2003
Genetics answers questions on the origins of life; how all living organisms adapt and reproduce by means of constant evolution.  As fundamental to the creation of life from DNA to RNA to protein, is inevitable carcinogenesis; the evolution of cancer. 
This article explores the mechanisms of cancer outside of the widely accepted etiology of base-pair mutations in primary DNA sequences.  In the context of genetic evolution, as DNA has the intrinsic ability to replicate itself, it also has the ability to pass on genes of cancer susceptibility.  The question is to what extent does gene silencing play a role in cancer development.  
Epigenetic changes, occurring independent of primary nucleotide sequences, to promoter sequences by DNA methyltransferase silences a gene by methylation.  As we know, the human genome is nearly 97% methylized and not transcribed.  In this respect, abnormal methylation results in cancer development in any of two ways.  Key genes essential for tumor suppression are methylized, or normally methylized DNA in noncoding chromatin become unmethylized.  Oncogene transcription as a result from abnormal unmethylization is a known cause of cancer.  Conversely, the article focuses on hypermethylation of promoter sequences of tumor suppressing genes and this as a mechanism of an inherited, epigenetically produced pathology.  Further understanding of the role of promoter sequence methylation has expanded treatment options for patients diagnosed with cancers of these origins.  These key elements to one of the most pervasive pathologies are explained to great length in this journal article as are the implications of basic genetic components in relation to cellular homeostasis.

Designing Babies: A Eugenics Race with China?
By Eric G. Swedin
Futurist, Vol. 40, Issue 3, pp. 18-21, May/June 2006
            This article is about accelerating the evolution process through engineering of the human genome.  The article raises the questions:  Is it wrong that China is removing children with birth defects in the population through early detection and abortion?  Is it good to disturb the natural evolution process?  Do we really want everyone to be engineered to perfection?  Will eugenics cause more harm than good?
            I think this article would be good to read in class because it involves the future of genetics.  This article is about altering genes to create the "perfect" person.  As genetics students, we should know how what we learn in class applies to the real world.  We need to understand how important DNA and genes are, and how they can be altered.  Genetic engineering could happen in our lifetime.

Association study of seven polymorphisms in four serotonin receptor genes on
suicide victims

Author’s names:
Videtic A, Pungercic G, Pajnic IZ, Zupanc T, Balazic J, Tomori M, Komel R.

Journal Title:
American journal of medical genetics. Part B, Neuropsychiatric genetics

Volume: 67 issue:1
Pgs: 669-672
Year: 2006

The question posed by this article was whether particular seritonergic
receptor subtypes were associated with suicidal behavior. In this experiment,
scientists studied if there was an association between the polymorphisms in the
5-HT receptor genes (1A, 1B, 1F, and 2A) and suicidal behavior on a sample of
226 suicide victims and 225 healthy control subjects. It was meant to disprove
that polymorphisms may be a genotype marker predictive of an increased risk for
suicidal behavior. The results of this experiment could have strongly suggested
that it is possible to determine suicidal behavior from one’s genes. The
article would be interesting in class because it raises the question- if we
could predict whether someone was likely to kill themselves, what would we as a
society do with this information? It would be fascinating to question and
analyze our society and what information regarding genes as a possible method
of diagnosing and, more importantly, predicting disease would cause us to do.
Through the experiment, no statistically significant differences of geneotype
distribution between the suicide and the control groups were determined from any
of the tested polymorphisms. The data was again sorted according to whether the
suicide was violent or non-violent and again no differences were detected.
However it was determined that the homozygotic genotype TT was present only in
the group of suicide victims, both violent and nonviolent. The data seems to
disprove the hypothesis that one’s genes for seritonergic receptor subtypes
were associated with suicidal behavior.

“Clinicogenetic study of mutations in LRRK2 exon 41 in Parkinson's disease patients from 18 countries”. Hiroyuki Tomiyama, Yuanzhe Li, Manabu Funayama, Kazuko Hasegawa, Hiroyo Yoshino, Shin-Ichiro Kubo, Kenichi Sato, Tatsuya Hattori, Chin-Song Lu, Rivka Inzelberg, Ruth Djaldetti, Eldad Melamed, Rim Amouri, Neziha Gouider-Khouja, Faycal Hentati, Yasuko Hatano, Mei Wang, Yoko Imamichi, Koichi Mizoguchi, Hiroaki Miyajima, Fumiya Obata, Tatsushi Toda, Matthew J. Farrer, Yoshikuni Mizuno, Nobutaka Hattori. Movement Disorders, Volume 21, No. 8, pg. 1102-1108, 18 April 2006.
This study concentrated on the three identified mutations of the LRRK2 exon 41 in different groups of people with Parkinson’s disease around the world (18 countries , 5 continents) and how the mutations are expressed in those groups (phenotype and genotype relationships). For example, in Caucasian subjects, a certain mutation (G2019S) exhibited a single-founder effect but did not in Japanese subjects; the I2020T mutation had a single-founder effect on the Japanese subjects. Furthermore, most of those with PD also had dementia and psychosis, and a link could possibly be investigated.
I feel that this study would be interesting in class because there is much recent interest in the inheritance of neurodegenerative diseases such as Parkinson’s. On a personal level, many students know of family members (grandparents, etc.) with PD or Alzheimer’s. With a genetic link, it could become an inherited possibility later in the lives of the students and their parents. Understanding the causes also increases research for possible treatments and prevention. It is also a personal choice of the individual as to which course of action, if any, they want to take, especially since genetics are merely chances and not necessarily a fate or guarantee.  I also feel that the scope of the study was unique. In the melting pot culture of the University of Texas and America in general, genetic differences are of interest in different demographics of people. Beyond race, since this study was done in drastically different areas, it could lead into inquiries of environmental factors and their effects on Parkinson’s disease such as diet. Also, the far-reaching distributions of mutations could lead to questions about the origin of this mutation (independent or common).

"Differential Gene Expression in the Lymphocytes of Malnourished Children" by Cristina Gonzáleza, Haydeé Gonzáleza, Leonor Rodrígueza, Leticia Cortésb, Oralia Nájerac, Fidel Hernández-Hernándezb, Luis Floresd and Edmundo Bonillaa.
Cell Biology International Volume 30 Issue 7 (pages 610-614). July 2006.

Summary of Article:
The article as published by the various authors above seeks to further expand on previous research done on varying gene expression between relatively healthy children and children suffering from marasmus type (40%<) protein-energy malnutrition. Citing various sources they note that PEM (protein-energy malnutrition) globally is responsible for more than 55% of deaths among children ranging from ages 1 to 4 years. Ultimately, the researchers sought to find whether or not prolonged malnourishment had a statistically significant effect on the gene expression of children and if (in the scenario that such changes did occur) how these changes affected the individual and if they acted as potential survival mechanisms.  With the authorization of the Ethics Committee of the Hospital Gustavo Baz, Netzahualcoyotl, Estado de México, the researchers took blood samples from 2 groups of children - 1 composed of well nourished children infected with a relatively common bacteria and another group of children that suffered from both malnourishment and the same infection. The lymphocytes of the blood samples were processed via electrophoresis and the resultant DNA analyzed. The results among the malnoursihed showed a particularly great down-regulation in mexatin and zinc-finger gene expression leading to decreased production of tumor necrosis factor (a substance that promotes spontaneous cell death) as well as to decreased production of a certain family of glucocorticoids that normally surpress T Cells. The decreased production of these two regulatory substances leads to relatively greater immune system efficiency and lower immunosupression than one would expect for individuals suffering from severe malnutrition, implying that the altered gene expression serves as a survival mechanism to protect the individual from infection while the individual is in a vulnerable state.

Why I chose this article: Gene expression at first glance seems to serve a relatively straightforward and unbending purpose; decoding the "pre-programmed" genetic information into living organic tissue that later reproduces itself with the next generation. However, the fluidity and practical purposes under which gene expression can serve also are just as important to the survival of the individual and species as a whole. Even under extreme duress, life finds a way to adapt within a single generation through varied gene expression; this implies that it may be possible (with sufficient knowledge) to manipulate the gene expression of an individual to increase survivability temporarily (for example in a famine an individual may exhibit survival mechanism against ineffection) until the crisis passes - a possibility that certainly merits further investigation.

Genetic Prediction of Future Type 2 Diabetes, Lyssenko V, Almgren P, Anevski D, Orho-Melander M, Sjogren M, et al, PLOS Medicine, Volume 2, November 1, 2005.
The questions posed in this article are as follows:
Do the genes PPARG and CAPN10 code for type 2 diabetes? 
            Can these genes serve as a means for screening the population for T2D?
I believe that this would make a good article for us to study in class because it is another nature vs. nurture situation.  Obesity has been around for many years, but now it has reached a peak in the United States.  I believe that this is an issue of growing concern for Americans, and as such would make for a good topic of study. 
This article displays results from possibly the largest to date study of its kind, and reveals that certain people are genetically disposed to developing adult onset diabetes.  People expressing certain phenotypes and having specific genotypes that are believed to be predisposed to T2d are tested.  The results are analyzed in depth and the targeted alleles are explained.  This article leaves much left to be studied; such as why exactly these particular genes influence development of T2D, but nonetheless studying this article would help people understand that adult onset diabetes is a hereditary, as well as an environmental, disease.

“Association of GABRA2 with Drug Dependence in the Collaborative Study of the
Genetics of Alcoholism Sample” , Arpana Agrawal, Howard J. Edenberg, Tatiana
Foroud, Laura J. Bierut, Gerald Dunne, Anthony L. Hinrichs, John I. Nurnberger,
Raymond Crowe, Samuel Kuperman, Marc A. Schuckit, Henri Begleiter, Bernice
Porjesz and Danielle M. Dick, _Behavior Genetics_, Vol. 36, No. 5, pg.640-650,
September 2006.

This study examines the connection between alcohol dependency and illicit
drug dependency possibly sharing genetic factors. The connection between the
two have been observed but the biological inherent genes have not been yet
associated. The method used by this study involves the use of multiplex
families affected by alcoholism, and the investigation also involved second and
third degree relatives. Genetic predisposition for alcoholism is weighted at
50-60% and the possibility of other dependencies such as cannabis (marijuana),
opioids (heroin, opium, etc..), cocaine, stimulants, and sedatives are at a
high likelihood of being in genetic association with alcoholism.

They proceed to examine this correlation more in depth by setting two goals.
The first goal was to find out if specifically, marijuana is in any way linked
to GABA receptor gene clusters located on chromosome 4 . And the second goal
they set out to achieve was finding out how much influence each gene on the
GABA gene cluster had with respect to the connection. The following genes :
GABRA2, GABRA4, GABRB1, and GABRG1, were all used in this study and were
quantitatively compared.

Blood samples were collected from the participants and taken for DNA
analysis. With the use of SNP pronounced as “snips” and genotyping in certain
regions that are already associated with alcoholism, they were able to get
comparable results. SNPs, short for Single nucleotide polymorphisms are DNA
sequence variations that occur when a single nucleotide in the genome sequence
is changed or altered and can occur in both coding regions or exons. In this
study both regions were taken into consideration. Since the majority or 99% of
DNA is very much the same for humans, the 1% that isn’t is very important in the
understanding of how this variation affects diseases and may include drug
dependence and alcoholism. SNPs are stable so using multiplex families would
not in any way distort the data since they do not change very often. Tests such
as the Pedigree Disequilibrium Test (PDT) was used to allow for the
consideration of larger families so that the data would be statistically
correct. To obtain the phenotypes a interview format was used and the
percentage of individuals with different combination of alcohol and drug usage
were sorted. Of the many SNP used, 4 with GABRA2 were strongly related to with
Alcoholism and also surprisingly were associated with drug dependence such as
marijuana and others. The other genes, GABRA4, GABRB1, and GABRG1 did not
present any compelling data. The interest was focused on GABRA2 which showed
much promise continued in a succeeding study using a much more case-controlled
method in order to get good data. The final conclusion of the study clearly
shows that GABRA2 is very much associated with illicit drug dependencies and
more specifically that it is narrowed down to individuals that used drugs in a

This article was very informative and actually has some serious relevance in
that alcoholism and drug dependence are addictions that may be life threatening.
The article shows the correlation between both addictions and is a very
important step in a series of many more steps to come for finding a valuable
treatment that will help millions who have to cope with this debilitating
disorder. Learning more about the genetics of such dependencies can help in
utilizing this resourceful information for possibly making better choices so
people can lead normal and healthy lives. It focuses on behavioral genetics
showing that genes have an influence over actions and manners of individuals.
This article adds to the debate between nature and nurture. Alcoholism and drug
dependencies once though to be mostly influenced by environment now shows that a
very significant genetic predisposition also exists.

Article Title: Genetic technologies, health care policy and the patent bargain
Authors’ Names: Caulfield TA, Knoppers BM, Gold ER, Sheremeta LE, Bridge PJ
Journal Title: Clinical Genetics
Volume: 63
Pages: 15-18
Date of Publication: September 27, 2002
This article talks about the moral controversy involved with patenting and privatizing the human genome.  The authors point out how companies and private organizations are well within their legal realm when they patent genes and that such privatization encourages innovation, but they also point out the complications that can occur in public health policy; they accomplish this by referring to a recent issue in Canada where a company that patented a portion of the human genome set the price for other companies to be able to use that specific portion too high.
I think this is an extremely interesting topic that is often overlooked by the mainstream media, policymakers, and, of course, the apathetic.  In this world where we are taught that public is bad and private is good, it is important to realize that there are exceptions to every rule.  People don’t think of the human genome as something to be privatized, and it would be enlightening to discuss the pros and cons of the patent controversy.

Major histocompatibility complex class II variation in the giant panda (Ailuropoda melanoleuca), QU-HONG WAN, LIANG ZHU, HUA WU and SHENG-GUO FANG,  Molecular Ecology, Volume 15, pgs. 2441 – 2450, published March 6, 2006
I thought that this article was very interesting because its main focus is animals whereas most of the genetic problems that we have been dealing with have had to do mainly with helping humans.  It deals with a genetic approach to problems with endangered species, mainly the panda, and not people.   It is a well known fact that DNA can be acquired from a blood sample of an individual.  But when the individual is a giant panda, a less invasive way to get the DNA would be much better.  The most noninvasive way possible would be to draw DNA from something that the individual has left behind, such as feces.  Feces is covered with cells from the intestinal walls of the animal and therefore is actually a very accurate way to get DNA, as long as it is acquired by minimizing genotyping errors.  I haven’t heard of many animals who usually get their DNA acquired this way, and I think it would be a good idea for people to start trying to find ways that are noninvasive, such as this way, to acquire DNA.  It would be just as accurate, but minimal pain.  Another issue this article talked about was how lack of MHC variation makes creatures more susceptible to disease, this is especially important for endangered species.  Currently most scientists are trying to increase the population of endangered species by mostly environmental means.  I think it would be a good idea to approach this problem with a more scientific approach. I don’t know how, but maybe there is some medicine that can be developed to make endangered species have a higher MHC variation.  Although, on a different note, some of the low MHC variation in endangered species is due to the bottle neck effect.  Because the pandas have been mating within themselves, they have similar genes and therefore smaller variation in MHC.   Pandas that are part of a larger group have more MHC variation because there is more of a genetic variety.  Forcing pandas to mate outside of their clan and form larger groups, and therefore more variation, would be more difficult than finding a scientific solution.  This experiment showed that there was small variance in the alleles found in the pandas.  There were fewer alleles actually found than were predicted to be found.  But, even though there wasn’t much variation between the alleles found, in some cases there were large differences within the alleles.  In the smaller groups there wasn’t much variation within the alleles and in the larger groups there was.  I think its interesting even though there isn’t much variation in the alleles, its possible for there to be a lot of variation within the alleles.  

Article Title: “In vitro selection of halo-thermophilic RNA reveals two families
of resistant RNA”
Authors: Jacques Vergne, Jean A.H. Cognet, Eörs Szathmáry and Marie-Christine
Journal: Gene, Volume 371, Issue 2, Pages 182-193
Date of Publication: April 26, 2006

Summary of Article:

This article demonstrates the idea of RNA being an integral part of the
evolution of life during the primitive years of the new world. The RNA World
Hypothesis, as we learned in class, proposes RNA as the first biological
molecule. A test was done to see if RNA is sensitive to temperature. In this
experiment, RNA molecules were exposed to high temperatures in high salt
concentrations to see how resistant they were to these environments, which were
similar to the environments of the early world. Systematic Evolution of Ligands
by Exponential enrichment (SELEX) is an in vitro evolution method in which the
RNA molecules were tested. Through this method, the molecules were heated
through multiple selection cycles, cloned, sequenced, and measured to see how
resistant they were when placed in extreme conditions. The results showed that
the resulting RNA molecules were grouped as two different families (I and II).
These families differed in secondary structures of the RNA and thermostability.
In family I, the secondary structures were longer and more stable than those of
family II (to make up in lack of stability, selected sequences better replicated
than those of family I). Also, a majority of molecules in family II degraded
during the heating process whereas a majority in family I remained intact.
This shows that family I RNA is stable enough to store and preserve sequencing
information for future generations while family II may be unstable and degrade
at high temperatures, yet the RNA molecules here carry information that make
replication easier. Therefore, this experiment helped demonstrate how survival
and reproduction are essential in biological evolution, through which RNA
remained resistant to degradation from high temperature while situated in high
salt concentrations.

The reason why I chose this article was to learn more about the RNA World
Hypothesis since my previous biology classes had not mentioned it. I think
this article provides us with more information on how RNA survives and how
different factors such as heat and concentrations can affect it. On a more
personal note, the beginnings of life on Earth have been a constant wonder for
me, and I am sure I am not alone with this thought. If RNA provided a pathway
for the first organisms to appear on the planet, then I think it is worth
learning more on how such a phenomenon can occur.

“Single-Nucleotide Polymorphisms in NAGNAG Acceptors Are Highly
Predictive for Variations of Alternative Splicing”, Michael Hiller, Klaus Huse,
Karol Szafranski, Niels Jahn, Jochen Hampe, Stefan Schreiber, Rolf Backofen,
and Matthias Platzer, The American Journal of Human Genetics, volume 78, pages
291-302, February 2006.

The article I read, entitled “Single-Nucleotide Polymorphisms in NAGNAG
Acceptors Are Highly Predictive for Variations of Alternative Splicing”,
obviously suggests that certain sequences of nucleotides may code for the
acceptance of a spliceosome on that binding site in the pre-mRNA, which would
lead to a form of alternative splicing. To begin, it should be explained that
the NAGNAG sequence represents codons in which “N denotes A, C, G, or T in
mRNA” (The American Journal of Human Genetics). Additionally, this article
elucidates that Single-Nucleotide Polymorphisms, or SNPs, are the “most
abundant form of genetic variation, contributing significantly to phenotypic
individuality and disease susceptibility” (The American Journal of Human
Since it is known that codons located within the coding regions of mRNA each
code for a specific amino acid within a protein, the idea that an alteration of
amino acid sequencing may cause problems, such as disease or early sequencing
termination, seems obvious. The extent of this effect, however, is widely
variable. Due to the redundancy of the genetic code, as there may be 3 codons
that code for the same amino acid, certain SNPs may not create these problems.
This article, however, argues the point that these SNPs can also influence
splicing, by dictating the point on a pre-mRNA in which a spliceosome binds and
begins splicing. Through a comparison of the human genome to the genome of a
chimpanzee, several plausible and implausible SNPs were determined. Of these,
95% of the “tandem acceptors match the consensus HAGHAG (H denotes A, C, or T)”
(The American Journal of Human Genetics), therefore rendering the HAGHAG as the
most plausible combinations of SNPs. Even a change of a “normal acceptor to a
plausible NAGNAG acceptor by a single mutation is sufficient to enable
alternative splicing” (The American Journal of Human Genetics).
The article goes on to mention that “recently, splicing mutations have been
suspected to be the most frequent cause of hereditary diseases” (The American
Journal of Human Genetics). Therefore, the study of these SNPs seems to be
extremely important. As the article provides data of experimentation performed,
it shows that of these plausible SNPs, several can create alternative splicings
that can lead to diseases such as Sjogren syndrome, Alzheimer disease, and Down
The reason this article would make for an interesting discussion in class is
that Alzheimer disease and Down syndrome are two of the most common ailments
affecting the human populations in the world today. I know that as I
read/watch/listen to the news, stories of advances made in Alzheimer’s research
that may ultimately lead to a cure for this devastating disease are common.
Until now, however, I never really felt like I had the resources to understand
exactly what these advances were, and how they were made. Since we have
recently discussed alternative splicing and it’s potential effects in class, I
feel that this article would be a perfect supplement to the curriculum.
This article touches on the exact implications of alternate splicing in a
relatively accessible manner, relating its initiation to the presence of a
particular sequence of nucleotides. In studying this article, it seems to
possible to understand how crippling diseases such as Alzheimer’s manifest
themselves within individuals. Understanding Alzheimer’s on the genetic level
would provide the class with a practical knowledge that could be applied to
better understand diseases that affect so many people each year. Therefore, I
believe this article would provide a good basis of study in our class.

Mutations in the gene encoding fibroblast growth factor receptor-3 in achondroplasia, Francis Rousseau, Jacky Bonaventure, Laurence Legeai-Mallet, Anna Pelet, Jean-Michel Rozet, Pierre Maroteaux, Martine Le Merrer & Arnold Munnich, Nature, 371, 252-254, 15 September 2002
Raises the question of the origin of achondroplasia, characterized by dwarfism in humans. The gene responsible for achondroplasia has been mapped to chromosome 4pl6.3, and it seems the mutation of a single amino acid account for all cases of achondroplasia in the series. 

An RNA gene expressed during cortical development evolved rapidly in humans,
Katherine S. Pollard, Sofie R. Salama, Nelle Lambert and more, Nature 443,
167-172(14 September 2006),

In this research, authors attempted to identify the possible sources of the
development of human-specific brain. They began by comparing our genome to that
of the chimpanzee and found the “human accelerated regions”, HAR1F and HAR1R, in
non-coding regions of RNA. In human, these RNA genes are expressed at a very
crucial time and place in the development of the cortex, an area where there
has been significant divergence since our last common ancestor with chimpanzee.

The article closely relates to our topics in that it deals with RNA and its
significant role in affecting the development of human-specific structures. I
found this article very intriguing because not only does it uncover the truth
of the development of our uniquely designed brain, but it also suggests the
potential methods for analyzing the key events of the human evolution. It could
help our class to understand the concept of RNA expression by providing
real-life examples and connecting the dots in the big picture.

Article Name: Distinct Clinical Phenotypes Associated with a Mutation in the
Mitochondrial Translation Elongation Factor EFTs

Authors: Jan A. M. Smeitink,* Orly Elpeleg,* Hana Antonicka, Heleen Diepstra,
Ann Saada, Paulien Smits, Florin Sasarman, Gert Vriend, Jasmine Jacob-Hirsch,
Avraham Shaag, Gideon Rechavi, Brigitte Welling, Jürgen Horst, Richard J.
Rodenburg, Bert van den Heuvel, and Eric A. Shoubridge

Journal: American Journal of Human Genetics, September 15th 2006

Description: I chose this article because it was about phenotypes that can
mutate in mitochondrial translation elongation factor (EFT). The genetic basis
for a mitochondrial protein-synthesis defect associated with a combined
oxidative phosphorylation enzyme deficiency was investigated in two patients.
The data proves that mutant EFTs were the cause of disease in both patients.
The overall idea that a mutation causes a disease or disorder parallels what we
have leaned in class. The article has a lot of technical terms that are very
hard to understand, but the overall theme is very interesting.

Title: Association of a functional serotonin transporter gene polymorphism with binge eating disorder
Authors: Palmiero Monteleone, Alfonso Tortorella, Eloisa Castaldo, Mario Maj
Journal: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics
Volume: 141B Issue 1
Pages: 7-9
<>Date of Publication: Oct 25, 2005
<>The reason I chose this article and why I think it will be of particular interest to the class is simply because, after all, we are college students and we know all about eating, particularly unhealthy. Once I saw this article, I got to thinking...could my excessive eating habits be something that is genetic? I mean come on, we all get hungry but for some reason it feels like nothing can ever satisfy my hunger as I am always indulging myself in mass quantities of food every couple hours. This article examines whether the polymorphism of the promoter of the 5HTT gene (5HT is brain serotonin), consisting of two variants a long and short, are associated with binge eating. No other case has been setup that has tried to show the correlation between 5HTTLPR and binge eating disorder. Therefore, case studies were setup that showed differences in 5HTTLPR genotype and allele frequencies between patients with the disorder and normal healthy weight subjects as well as possible relationships between 5HTTLPR and phenotypic variables.

Comprehensive splice-site analysis using comparative genomics,
Nihar Sheth, Xavier Roca, Michelle L. Hastings, Ted Roeder, Adrian R.Krainer and
Ravi Sachidanandam, Oxford Journals: Life Sciences; Nucleic Acids Research, Vol.
34 Number 14, pgs. 3955-3967,August 12,2006

The main question that is posed in this journal is the identification of
the naturally-occurring splice sites that help to give insights into pre-mRNA
splicing. The concept of alternative splicing is not agreeable to an
analysis based solely on splice sites. In order to identify common and
distinguishing features in each splice-site type, the researchers have
collected and analyzed a comprehensive set of naturally-occurring splice sites
from the genomes of five model organisms, through this they will reach a greater
understanding of complete splice-site analysis using comparative genomics.
I think that this article will be an interesting one to study in our
class because it builds on a topic which we have covered (introns, exons, and
splicing) and makes for a real experimental understanding of the concept and
how the process works. With a new understanding on topics we have never heard
of before.

The group of researchers listed above have collected over half a million splice
sites from five species: which include:Homosapiens, Musmusculus, Drosophila
melanogaster,Caenorhabditis elegans and Arabidopsis thaliana—and classified
them into these four subtypes: "U2-type GT–AG and GC–AG and U12-type GT–AG and
AT–AC." They have also
found new examples of uncommon splice-site categories, such as U12-type introns
without canonical borders, and U2-dependent AT–AC introns. For the U12-type
introns, they found several features conserved across species, as well as a
clustering of these introns on genes. Using the information content of the
splice-site motifs, and the phylogenetic distance between them, they identified
through there research: "(1) a higher degree of conservation in the exonic
portion of the
U2-type splice sites in more complex organisms; (2) conservation of exonic
nucleotides for U12-type splice sites; (3) divergent evolution of C.elegans
3' splice sites Their study proves that the identification of broad patterns in
naturally-occurring splice sites, through the analysis of genomic datasets,
provides mechanistic and evolutionary insights into pre-mRNA splicing."
Historically, splice sites are ranked, based on compilations of splice sites.
However, none of these ranking schemes accurately identify the bona fide splice
sites. In addition, alternative splicing, involving the choice of competing
splice sites, is not amenable to an analysis based solely on splice sites. In
order to identify common and distinguishing features in each splice-site type,
the researchers have collected and analyzed a comprehensive set of
naturally-occurring splice sites from the genomes of five model organisms: Homo
sapiens, Mus musculus, D.melanogaster, Caenorhabditis elegans and Arabidopsis
thaliana. They have revisited relevant themes in splicing, such as the
frequencies of U12-type and other rare introns, and the variations in the 5'
and 3'ss motifs among the five organisms.
The final results go into great depth of how the introns were classified into
various splice-site subtypes. And furthur how they were able to retrieve splice
sites by type. They came to the conclusion that this tool allows users to
retrieve splice site flanking sequences by specifying one or more splice-site
subtypes, cut-off 5'ss or 3'ss scores, and species. By using this tool one
will be able to locate potential protein-binding sites by searching for
sequences that match the patterns in the form of regular expressions.

Title of Article: An mRNA structure in bacteria that controls gene expression by binding lysine
Authors: Narasimhan Sudarsan, J. Kenneth Wickiser, Shingo Nakamura, Margaret S. Ebert, and Ronald R. Breaker
Journal Title: Genes and Development
Volume: 17
Page Numbers: pp 2688 - 2697
Date of Publication: Nov 2003
Description of Question Posed:
The description of the question posed here relates to the direct sensing of metabolites by messenger RNAs is a fundamental form of genetic control and that riboswitches represent a new class of antimicrobial drug targets.
Reason Why Article Should Be Discussed:
The article should be discussed due to the fact that most known genetic factors that respond to such environmental changes are proteins, but, in this experiment, it is shown that RNA molecules can also recognize small organic compounds and harness allosteric changes to control the expression of adjacent genes. These metabolite-binding RNA domains, termed riboswitches, typically are embedded within the 5' untranslated regions (UTRs) of mRNAs, and control the expression of proteins involved in the biosynthesis or import of the target compound. (e.g., see Mironov et al. 2002; Nahvi et al. 2002; Winkler et al. 2002a,b). By binding Lysine, the mRNA structure in the bacteria controls the gene expresson. It is termed “lysC”, and the lysC gene basically encodes aspartokinase II, which catalyzes the first step in the metabolic pathway that converts L-aspartic acid into L-lysine (Belitsky 2002). This article is vital and should be discussed because the data from the study strongly support that a lysine-responsive riboswitch might serve as the genetic control element for this gene, and that riboswitches represent a new class of antimicrobial drug targets.

Genome Survey for Loci That Influence Successful Aging: Results at 10-cM
Resolution, George S. Zubenko , M.D., Ph.D., Hugh B. Hughes III, M.S., Wendy N.
Zubenko , Ed.D., A.P.R.N., Brion S. Maher , Ph.D, American Journal of Geriatric
Psychiatry, online, August 11, 2006.

This article is asking about the genetic differences between the very old and
the young. It asks—is there some genetic difference in the people that grow
very old that allows them to do so? Or, is there something in the genes of
young people that predetermines that they will never live into old age? George
Zubenko, a professor at the University of Pittsburgh School of Medicine compared
the DNA of 100 men and women who had reached the age of 90 while still
maintaining mental cognition with the DNA of 100 young adults with similar
proportions of sex and race.
The study found several interesting differences between the genes of the young
and the old. The older people were much more likely to have the APOE E2 allele
and much less likely to have the APOE E4 allele than the group of young adults.
Zebenko also discovered nine new genetic regions specific to men or women that
are believed to be associated with successful aging. Most of these regions
overlap with regions that are linked to cardiovascular and other disorders, and
the presence of these “successful aging genes” is believed to inhibit those
disorders. The article also touches on the nature vs. nurture debate on aging.
The study found that those who did not smoke or drink were much more likely to
live into old age.
This article would be interesting for class because everyone wants to live into
old age. This was just published, and it has the most current ideas about what
it is that allows some people to live so much longer than others.
Theoretically, we could all have our DNA examined for the traits described in
the article and see if we have the genetic predisposition to live into our
nineties—which sounds pretty interesting/scary to me.

BY GENETIC DRIFT, Reinaldo A. de BritoA, 1, L. Susan PletscherA, James M.
Cheverud, Evolution Vol. 59, Issue 11 pp. 2333–2342 (November 2005)

In searching for the relationship between the evolution of genetic architecture
and genetic drift, researchers tested the breeding value of four standard
inbred mouse strains mated across a set of recombinant lines generated from the
intercross of the two different inbred mouse strains. The result showed that
there is strongly significant interaction for all traits which means the traits
were differentiated by genetic drift during the production. Also, it suggested
that common patterns of selection in these differentiated populations could
result in the fixation of different alleles.

I honestly could not fully understand the result of the experiment since I
barely have any knowledge regarding the complicated multi-cross between sets of
different traits. Some analysis, however, was familiar since it involved the
basic concepts of the genetics, such as the founder effect and the genetic
drift. I believe studying this article and topic could lead us to in-depth
analysis of the evolution of genetic architecture and its impact on genetic

“Re-analysis of Collaborative Study on the Genetics of Alcoholism pedigrees
suggests the presence of loci influencing novelty-seeking near D12S391 and
D17S1299.” David Curtis. Psychiatric Genetics, Vol. 14 Issue 3, p151-155,

Are human personality traits heritable? Previous analysis of 758 sibling pairs
from families of alcoholic found evidence for linkage harm avoidance to markers
on 8p21-23, and this study was supported by other linkage study of 384 sibling
pairs. The tri-dimensional personality questionnaire about novelty-seeking,
harm-avoidance, and reward-dependence was used to study influence of genetic
variants to these traits. There have been two previous linkage studies of
these personality traits. The first one was carrying out genome scan of 758
sibling pairs from 177 alcoholic nuclear families. This experiment showed that
linkage of harm avoidance is marked on 8p21-23 with additional markers on 18p,
20p and 21q. The second experiment provided the evidence of markers on 8p21,
1q21-24, and 22q12-13.
The dataset of 105 pedigrees containing 1214 subjects is collected for
Collaborative Study on the Genetics of Alcoholism. The pedigrees are selected
for having three or more members affected with alcohol dependence and provided
with tri-dimensional personality questionnaire. Linkage analysis of the three
personality traits was carried by lod score analysis of quantitative traits
implented in the QMFLINK program. For each test, likelihoods are calculated
for a range of transmission models. Also for each pedigree likelihoods were
calculated under condition of linkage and non-linkage.
Through the results, it was clear that trait of novelty-seeking was more
heritable traits than harm-avoidance and reward-dependence. And
Reward-dependence produced result of least related linkage traits.
Linkage between traits and genetic variance is controversial. Many positive
and negative experiments were carried out, but lack of consistency in the
results gives difficulty in drawing conclusion.
This research will make class interesting since people usually believe that
main component of building personality is environment. This research
investigates how one gene can builds up person’s certain characteristics. This
study raises question of nature vs. nurture. Are characteristics and
personality genetically heritable, or are nature and nurture interrelated to
build up person’s characteristics? Genetic class will have a lot of fun by
investigating these questions.

Mother knows best: Epigenetic inheritance, maternal effects, and the evolution
of human intelligence
Developmental Review
Volume 26, Issue 2, June 2006, Pages 213-242

The article written by David F. Bjorklund focuses on a new part of genetics
that we have yet to discuss in class. It is called epigenetic inheritance.
Epigenetic inheritance deals with changes in gene functions without a change in
the DNA sequence. This field in genetics is unique because most of what we
research is done by comparing one generation’s genes to its ancestors, in which
physical differences can be traced. But what about behavior, personality, or
intelligence? We can obviously see the physical differences but mental
differences become much harder to trace genetically. The article briefly brings
up the idea of postnatal behavior using rats in their experiment. The experiment
used rats that were handled and nonhandled resulting in an offspring of
different natures. The handled rats were more active and curious to explore
environments than the nonhandled rats. This answers the question to whether you
can link behavior genetically through generations. It was found that the gene
linked to the activeness in the rats was found in it’s ancestors, the
C57BL/BALD strain.
Another experiment in the same article linked licking and grooming and
arched-backed nursing (LG-ABN) to behavior in their offspring. Children from
families with high levels of LG-ABN are less stressful than offspring with
lower levels of LG-ABN. When the children were switched to foster parents,
their stress resembled that of their foster parents than maternal. After
inheriting the behavior from the foster parents, it was found that the same
behavior was passed down at least 2 more generations. Conclusively, individuals
differ in behavior because of variations in care. This idea belongs with the
nature vs nurture idea about sexuality and how one is brought up in society,
providing more positive evidence to support the reasoning.

Age and Apolipoprotein E*4 Allele Effects on Cerebrospinal Fluid -Amyloid 42 in
Adults With Normal Cognition

Elaine R. Peskind, MD; Ge Li, PhD, MD; Jane Shofer, MS; Joseph F. Quinn, MD;
Jeffrey A. Kaye, MD; Chris M. Clark, MD; Martin R. Farlow, MD; Charles DeCarli,
MD; Murray A. Raskind, MD; Gerard D. Schellenberg, PhD; Virginia M.-Y. Lee, PhD;
Douglas R. Galasko, MD

Archives of Neurology. July 2006;Volume 63:936-939.

The objective of this research article is to determine the effects of normal
aging and the presence of the APOE*4 allele on A beta 42 protein concentration
in spinal fluid of adults. Alzheimer's-related plaques composed of A beta 42
proteins begin to form on the brain years before any symptoms of the disease
are shown. Due to the clumping of the A beta 42 protein into plaques on the
brain, there will be less of this protein in spinal fluid. Therefore, a
decreased level of A beta 42 in the spinal fluid can indicate the development
of Alzheimer's. This study found that older people with the APOE*4 allele are
more likely to have lower levels of A beta 42, than those without the allele.
People with the APOE*4 allele showed a slight decline in the A beta 42
concentrations at a much earlier age, followed by a dramatic delcine from 50-60
years old. Researchers report that people with the APOE*4 develop 'clinical
dementia' 10-15 years sooner than those without it.

“Type 2 diabetes mellitus: from genes to disease”, Maciej T. Malecki and Tomasz
Klupa, Pharmacological Reports, Volume 57, Pages 20-32, 24 August 2005

The chosen article addresses the current status of Type II Diabetes Mellitus
(T2DM) research in terms of genetics. Malecki and Klupa report on the current
findings that relate monogenic mutations on the DNA to strong cases of the
disease. However, there are many exceptions to the findings; in fact, 90% of
cases of diabetes are found to be caused by changes at multiple loci. This is
further seen by the fact that cases of T2DM show that it can cause two
different effects: insufficient insulin secretion in the body and/or a decrease
in the ability of cells to take up the insulin. The genetic nature of the
disease is supported by the fact that there is a higher prevalence of diabetes
in monozygotic twins versus dizygotic twins and that there is a higher
frequency of diabetes in certain families. The big question that is partly
discussed, but never concluded upon is the argument over nature versus nurture.
Despite the findings of science, there is a variety of exceptions that reinforce
the environment’s role in determining the phenotype of the disease. Differences
in the prevalence of the disease based on ethnicity and geographic regions are
cited by Malecki and Klupa. At no point can they determine the specific affects
that nature or nurture plays in the determination of the gene.
“Environmental factors may be responsible for the initiation of â-cell damage or
other metabolic abnormalities, while genes may regulate the rate of progression
to overt diabetes. On the other hand, in some cases genetic factors may be
necessary for environmental factors even to start processes leading to the
development of the disease” [1].
The authors are unable to explain the polygenic appearance of certain cases and
instead speak about the clearer monogenic form. In monogenic diabetes cases,
there has shown to be a high chance that the disease will occur in the
individual. Such affected individuals are largely affected by their “nature”
over the environment’s influence, though they explain that the environment
still plays its role. These individuals have severe defects in their organs
that produce insulin and thus are the worst cases of type II diabetes.
Mutations affecting transcription and translation factors have been found. In
the case of those that affect transcription factors, nature plays a big role in
determining the appearance of the disease; most cases are severe and early
onset. In contrast, translation factors are highly affected by the environment.
Even in cases with the same monogenic mutation, the environment can be the
deciding factor in determining the appearance of the disease.
Another question that scientists continue to ask is about the pathway for
insulin within the body’s cells. There exist insulin resistant cells that are
also the cause of monogenic type II diabetes, but because insulin’s path and
its action on the cellular level is complex, it is relatively unknown.
Complex Type II diabetes, a more common form of the disease, has an unknown
interaction between genetics and environment. In cases with polygenic
inheritance of diabetes, there exist many loci that are said to be the causes
of the disease. The genes that cause the disease vary greatly and there has
been little success in relating the disease to any specific, universal loci
“The final number and the relative contributions of these genes are
uncertain…they may belong to the same or to different casual pathways. Some
genes may contribute substantially to the development of diabetes in one
population with no or limited effect in another ethnic group.” [2].
Even when signs of the disease exist genetically, the disease doesn’t
automatically appear. The goal of determining the loci that cause the disease
is extremely difficult because of environmental factors; there are cases where
there doesn’t seem to be any genetic link. In contrast, many individuals have
the genes that seem to cause the disease, but never express them due to
differences in environment.
This journal article is useful because diabetes is a disease that is highly
prevalent in most industrialized countries around the world. A more disturbing
fact is that the percentage of cases is increasing, especially in younger
people. Such questions bring about a more realistic issue to the topic of
genetics as many of us know someone affected by the disease. Diabetes also
causes a decrease in life expectancy of those that are affected by it and thus
it is a major health problem in our society.

Genomics of the future: Identification of quantitative trait loci in the mouse
Lorraine Flaherty1, Bruce Herron and Derek Symula
Genome Research
Volume 15(12)
pages 1741-5
2005 Dec

The article is about studying mice genes in order to help find diseases, find the particular genes that cause them, and also their positions in the chromosomes.  New technology in the field helps us do this research quicker and with more precision.  The article also goes over the new methods that can be used to help us solve these complex problems.  The article is interesting because it focuses on the future of gene research and what students might encounter in the field in a few years.

"Long-term gene expression changes in the cortex following cortical ischemia
revealed by transcriptional profiling" by Carola Krüger, Durmus Cira, Clemens
Sommer, Achim Fischer, Wolf-Rüdiger Schäbitz,and Armin Schneider
Source: "Experimental Neurology" Volume 200, Issue 1 , July 2006, Pages 135-152

The article is concerned with the molecular changes that are involved in a
post-cortical ischemia rat model that simulates stroke. The gene expression
patterns contribute to the neural reorganization after injury, but it has not
been fully explored how most of these regulatory genes actually affect injured
neurons. It is the purpose of this paper to more clearly define the role of
many genes shown to change following a photothrombotic ischemic injury induced
in the rat parietal cortex.
The issue of neuronal restructuring is a hot topic right now in Neuroscience
and the effects of regulatory genes in this process are beginning to be
understood. Regulatory genes are very important in sustaining life and often
the field of Molecular Biology seems to focus on genes as what forms an
organism and not as much on what sustains them also. This paper brings to light
the future of medicine in the potential for pharmaceutical gene therapy
replacing older methods like surgery in some cases or allowing medical
assistance to the injured or impaired where there was no hope before.
Neuroscience is a field that a lot of students are not exposed to very early
on but many find it interesting because of the complexity and because of how
much we know about the brain and how much we still do not know.

New gene construction strategy in T-DNA vector to enhance expression level of
sweet potato sporamin and insect resistance in transgenic Brassica oleracea,
Huai-Ju Chen, Shu-Jen Wang, Chien-Cheng Chen and Kai-Wun Yeh, Plant Science,
Volume 171, Issue 3 pg 367-374, Sept 2006

This article asks the question could a specific plant gene, sporamin, be
activated in sweet potatoes to make it more pest resistant? In experimentation,
the authors tried to see if adding a wound-responsive promoter or a DNA
attachment would encourage higher levels of sporamin. Through their results,
they found the subjects that contained both the attachment and the promoter
would display greater amounts of sporamin and therefore greater pest
resistance. They also found that in subsequent generations, the promoter and
attachment were stable and inheritable.
This article would be interesting because it talks of genetically modified
food and the stability that is being found in the modifications that can lead
to future benefits.

“Unraveling adaptive evolution: how a single point mutation affects the protein coregulation network”, Christopher G Knight, Nicole Zitzmann, Sripadi Prabhakar, Robin Antrobus, Raymond Dwek, Holger Hebestreit & Paul B Rainey, Nature Genetics, Volume 38 No 9,1015-1022, Published online: 20 August 2006
After reading this article I feel that the article leads the reader to think about some very significant questions that are either directly mentioned in the context of the article or brought about by the assumptions that the researchers make.  The most important questions that I found myself asking from reading this article were the following: “Is evolution still occurring in today’s species?”, :Can we see adaptive evolution in a controlled environment?”, ”Can we study evolution on the DNA level?”, ”How significant is a single base pair mutation on the entire organism?”, and “How does adaptive evolution affect the ecosystem?”.
The article shows evidence to studying the evolution in bacteria in a laboratory environment and from that occurrence I found myself asking two questions.  The first question I asked was, “Is evolution still occurring in today’s species?”.  I believe that species have evolved over time and after this question I was asking myself whether or not evolution was continuing to occur in today’s species.  It makes sense that species are constantly evolving and adapting if one adopts the mentality that evolution is in fact a legitimate explanation for our origins, but this article assumes that not only is evolution still occurring but it is also observable and recordable.  This assumption leads me to question whether or not adaptive evolution can be seen in a controlled environment.  Every biology student is taught about Darwin’s finches with different shaped beaks, but it is still a theory to why and how the beaks came to be.  In this controlled experiment the researchers go to show that they can record this bacteria adapting to its new niche.
 After I got deeper into the article it began to discuss the adaptive evolution of a certain bacteria and how they could see a difference between the genes of the old bacteria and the new, evolved bacteria.  This forced me to ask, ”Can we study evolution on the DNA level”.  This article seemed very confident that they could track the evolution from the old bacteria that stayed in the liquid to the new bacteria that made formed a boundary between the air and liquid in the DNA.  They found one mutation in one base pair and accredited the evolution to that one mutation.  The researchers believed that it was the forces of pleiotropy that made this one base pair affect so much on the entire organism and made me wonder, “How significant is a single base pair mutation on the entire organism”.  In this case the researchers found this one base pair to be very important to the entire organism, but how significant is each base pair.  Some base pairs probably control very important things such as this one must have, but others might not control things so important.
The last question I found myself asking was since these researchers found that this bacteria filled a new niche in the ecosystem that they made as a control environment, “How does adaptive evolution affect the ecosystem”.  This article leads me to believe that the mutation occurred first and that the new niche was filled second like the mutation caused the shift of niche.  I find it peculiar that the mutation forces the change rather than so much I have learned before, which assumes that a change in the environment forces a shift in the genes over a long period of time.  This article goes against what I had learned and stated that the mutation caused the shift and could be seen within the duration of their experiment.
Overall, I feel that this article has a lot of relevance to our class because it assumes a lot of things that people as a whole are not completely comfortable with.  I also feel that this article views evolution at both a genetic level and an ecosystem level, which goes to show the differences between the two ways of studying evolution, but also tries to connect the two to make the theory of evolution more solid.

Molecular analysis of flies selected for aggressive behavior, Herman A.
Derick and Ralph J Greenspan, Nature Genetics, pages 1023-1031,
September 2006

The authors of this article wanted to see whether flies selected for
aggression showed different expressions of genes. To find out they ran a
simple experiment where they started with a normal population of flies
from which they selected flies to make offspring. By selecting flies
that showed aggressive territorial behavior, such as fighting with and
tossing other flies, they created two populations of aggressive flies
over 20 generations. By also randomly selecting flies from the original
group they created two populations of neutral flies. After each
subsequent generation the aggressively selected flies’ offspring became
more and more aggressive. After over 20 generations, the two aggressive
populations fought more often, fought longer, and fought more intensely
than the two neutral populations, even though both types were equally
active in other activities. Surprisingly the aggressive flies mated less
than the neutral flies when they were in direct competition with one
another. The authors believed that this is due to the fact that in the
experiment mating was not linked territory. This find shows that
aggression only has evolutionary significance when taken in a
territorial context.

When the experimenters analyzed the RNA in the brains of the flies they
found there were eighty genes that were significantly expressed
differently between the aggressive and neutral populations. The
aggressive flies had higher expression of genes for muscle contraction,
CA2+ signaling, energy metabolism, and cuticle formation. These changes
in the genome the authors suggest allow the aggressive flies to fight
harder and longer than neutral flies.

After analyzing the differential expression of genes between the
aggressive and neutral flies the experimenters used some of these genes
in mutant flies to see if they produced an observable phenotypic effect
on aggression levels. They found that the gene that encodes for
cytochrome P450 produced a positive measurable effect on aggression. The
experimenters believe that this protein could be involved in pheromone
recognition of other male flies, which could lead to greater aggression.

This article is interesting because it showcases the two way interaction
of genes and the environment. After only a short period of time the
experimenters were able to radically alter the genome of the flies by
only selecting for one phenotypic trait. Likewise, the changes in gene
expression effected the flies’ interaction with the environment in
aggression and different tasks such as sexual competition.

The Use of Racial, Ethnic, and Ancestral Categories in Human Genetics Research;
Kate Berg, Vence Bonham, Joy Boyer; American Journal of Human Genetics 77.4
(Oct 2005): p519(14)

The concept of genetic differences between races and ethnicities give way to
conflicting ethical views. Some people believe that the whole concept of
researching genetic differences between races and ethnicities is useless
because of the major health differences that are caused by economical
differences within their society. There is also the questioning of stereotyping
these races and ethnicities by way of amplifying and exaggerating genetic
findings in order to give berth to genetic superiority or inferiority. On the
other side of the argument, races and ethnicities are exposed to different
environments all over the world. Researching their genetic makeup in these
different environments is a huge point for this side of deliberators when
wanting to find origins of diseases. I believe this is a very important issue
to be deliberated. This is a very ethical and sensitive issue, and one of which
that should be discussed within the classroom. It deals with the diversity of
humans genetically and their respective environments. Researchers try to figure
out if a connection between the two exists and what type of effects the
environment has upon the genetic makeup. Another question posed in the article
asked if races were classifying people unfairly and inaccurately. The
researchers also deal with discussing how researchers can modify their methods
in order to cool down the criticisms of this topic, such as broadening their
classifications. A proposal that arose from these discussions was ancestral
classifications. The author brings up another issue for Americans in that there
are many studies which propose the cause of major health issues between them.
They do not believe that these health problems are genetic as much as they
believe prejudice, poverty, and health care accessibility among other things.
When exploring the possibilities of disease rise, some researchers posed that
they might originate from combinations of rare cases of that disease through
different allele frequencies. This would be a great discussion in class because
of RNA editing and alternate splicing with the introns/exons.

DNA mimicry by proteins and the control of enzymatic activity on DNA
Dryden DTF
TRENDS IN BIOTECHNOLOGY 24 (8): 378-382 AUG 2006

DNA requires specific enzymes to bind with proteins to produce a useful
reaction. However there are competitor proteins that compete for the spot with
different proteins. However there is another interaction with the enzymes and
the control protein that blocks the interaction with the DNA and binding
enzyme. This type of interaction can occur in two ways: either indirect or
direct. One way to block the control protein to the binding site is to “mimic”
the natural substrate. The mimic has to have the same shape and electrostatics
that the enzyme would normally recognize. This type of mimicry is known to
occur upon DNA, including transcription, repair, and restriction. A profession
that has taken off with mimicry is the pharmaceutical industry. Mimicry in this
industry has created many new drugs for the public to use to their advantage.
DNA mimicry by proteins has advanced so much that nature isn’t stopping this
phenomenon. “The protein structures used by DNA mimics cover all know secondary
structure types-alpha helices, beta strands and peptide loops”. DNA mimicry has
come so far along that it can be performed either naturally or in the lab by
scientist. Mimicry can be used in the following of ways: it might be possible
to use DNA mimics instead of actual DNA molecules in the preparation of
co-crystals, labeling experiments for detection of target DNA-binding proteins
and their isolation using affinity methods, and finally mimics might be able to
target not only bacterial restriction systems but also other systems such as
replication, repair and drug resistance. The mimicry of a protein to compete
with actual natural protein to mimic its shape, size, and electrostatics to
beat it out of its spot is pretty amazing and scientists are only finding new
ways to mimic these substrates. In the future it is said, that they will have
proteins to mimic every site of binding for a DNA structure.