Dr. Reichler’s Bio 325   TTh 9:30-11am    Print Name:____________KEY________
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? (6 pts)
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 expressed.

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?
(6 pts)
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 unreplaced.

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 cancer? (8pts)
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 partner? (3pts)
When the other male has better genes than her mate.