Dr. Reichler’s Bio 325 TTh 9:30-11am
Exam #2 November 2, 2006
Read each question carefully and don’t hesitate to
ask if a question seems unclear. If possible, answer each
question in the space provided, but if needed, continue on the
back. If you use a drawing as part of your answer, be sure to
also include a written explanation. These questions have specific
answers, although for some, more than one answer is possible. To
receive full credit you must clearly and fully answer the question
being asked. This exam is worth 103 points with the points for
each question noted in parentheses.
1. Where in the vasopressin/oxytocin receptor gene would you expect to
find differences between prairie and montane voles? How would
this difference cause the different behaviors observed in prairie and
montane voles? (8 pts)
Any one of: Promoter/Enhancer-
different levels of transcription lead to different receptor that lead
to different behaviors. 3’ or 5’ UTR- differences in mRNA
stability. Coding region- changes in protein stability could lead
to different levels of the receptor.
2. Could a female who mates with only a single male be choosing that
mate based on compatible genes? Why or why not? (6 pts)
Yes, women prefer men with certain
HLA genes that indicate levels of compatibility.
4/6 pts No, there is no obvious
signs of compatibility, several genes may be involved that the female
may not be aware of in herself or her mate, so the only way to
guarantee compatibility is to mate with several males.
3. When having EPCs (extra pair copulations) with older males, are the
female purple martins with young male mates primarily obtaining good
genes or compatible genes? Explain. (6 pts)
Good genes. They are not having
EPCs randomly, but with males that have demonstrated their genetic
quality by surviving through several years.
4. What is a major weakness of the data obtained via microarray
analysis, and for what gene would a microarray not have this weakness?
Microarrays show differences in mRNA
levels, but that does not necessarily correlate to changes in protein
levels. (Second part of question is bogus. Full credit for
problem with microarrays.)
5. The trp operon in bacteria produces several proteins responsible for
the synthesis of the amino acid tryptophan. Would the repressor
of the trp operon bind to the trp operon promoter if the bacteria were
in the presence of plentiful tryptophan? Why or why not? (6 pts)
Yes, the proteins of the trp operon
are not needed to synthesize tryptophan if there is plentiful
tryptophan already present.
6. Would you expect the histones adjacent to the telomerase gene to be
acetylated in an adult’s brain? Why or why not? (6 pts)
No, histone acetylation unpackages
DNA in preparation for transcription. Telomerase is not produced
in an adult brain, the cells rarely divide, so telomerase is not
7. While looking at the expression of the mRNA for “stopthepain” (a
protein involved in responding to highly stressful situations), you
notice that the amount of mRNA does not change when the subject is
exposed to high or low stress, but the size of the mRNA does
change. What is different, and what is not different, about the
regulation of this gene in response to stressful situations?
Explain. (6 pts)
Different- alternate splicing
Not different (any of)- transcription
and/or mRNA stability
8. Would you expect the promoters for the Cdk and cyclin genes to be
similar or different? Why?
Different- Cdk is constantly
expressed while cyclin expression changes throughout the cell
cycle. Different promoters will allow different transcription
factors to bind, thereby leading to different expression patterns.
9. Do the gaps at the ends of DNA occur on the leading or lagging
strand? Explain. (6 pts)
Lagging strand. DNA polymerase
moves away from the end of the DNA leaving the last RNA primer
10. What are one similarity and two differences between DNA replication
on the leading and lagging strands? (6 pts)
Similarity (any one of)- Need RNA
primer. Start with Primase. Use ligase. Add
nucleotides at 3’ end. Reads template in 5’ direction.
Differences (any two of)
Leading strand: Continuous
replication. Need single primase, primer, ligase, DNA
polymerase. Follows helicase. No gap at end.
Lagging strand: Discontinuous
replication (Okazaki fragments). Need multiple primase, primer, ligase,
DNA polymerase. Moves away from helicase. Leaves gap at end.
11. What are three genes that might be over-expressed (overabundant) in
a cancer cell, and one gene that might be absent in a cancer
cell? How would the expression of each of these genes be a part
of leading to cancer and/or how would it make it difficult to treat the
Over-express (any three): Telomerase-
needed to keep DNA end erosion from destroying genes or stopping cell
division. MDR- can make chemotherapy ineffective by pumping out
drugs. Angiogenesis genes- attract blood vessels to supply
tumor. Cyclin- keeps cell cycle active. Any gene involved
in DNA replication.
Absent (any one): p53- kills cells
with DNA damage. DNA repair- recognizes and repairs damaged
DNA. Contact inhibition- cancer cells lack contact
inhibition. Cell Adhesion- in malignant cancers cells break off
and lodge in other parts of the body.
12. What gene would be differently expressed between a cell undergoing
mitosis or meiosis? What is the gene that is differently
expressed, and why is it expressed differently in the two cells? (6 pts)
Any one of: Genes involved in
crossing-over are not needed in mitosis. Genes that bring
homologous pairs together in tetrad as this does not occur in mitosis.
13. Would an organism that was always haploid be able to produce
genetically diverse offspring? Why or why not? (6 pts)
No, genetic diversity occurs during
meiosis, and only diploid cells can go through meiosis.
4/6 pts Yes, by mutations.
14. Are there many genes expressed during mitosis? Why or why
not? (6 pts)
No, tight packaging of DNA into
chromosomes means that most genes are not available for expression.
15. Does it matter how the sister chromatids line up during
mitosis? Why or why not? (6 pts)
No, the sister chromatids should be
identical, replicated DNA. BUT If there was a replication
error, it would matter.
16. Crossing-over and random assortment both increase the genetic
diversity of gametes, but the increased genetic diversity of a gene
caused by crossing-over would not have its genetic diversity affected
by random assortment. Why? (6 pts)
Crossing-over only affects genes on
the same homologous pair of chromosomes and random assortment only
affects genes on different chromosomes.
Bonus: When would a female looking for good genes be willing to
accept an EPC (extra pair copulation) with a male that is not her
When the other male has better genes
than her mate.