2008problemset10%20key

2008problemset10%20key - ProblemSet#10KEY(BICD100W08 1...

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Problem Set #10 KEY (BICD 100 W’ 08) Questions 1-4 deal with Ralph Greenspan’s lecture on March 5 th (lecture 23) – refer to the pdf version of his lecture slides and/or your notes as needed to answer the following questions. 1. What is the evidence that schizophrenia is a heritable trait in humans? See lecture 23 pdf pg. 8: a high correlation is observed for related individuals in the incidence of schizophrenia – the correlation increases with degree of genetic similarity, although it does not perfectly mirror degree of genetic similarity. For example, incidence of schizophrenia in individuals whose full sibling is schizophrenic is 9% vs. 6% for half siblings. Also, incidence for fraternal twins (17%) is much higher than for siblings (6%) even though their genetic relatedness is equivalent, perhaps suggesting some influence of maternal environment during gestation as seen for IQ testing ability. 2. What is one possible explanation for the lack of reproducibility in results obtained from different studies attempting to identify schizophrenia genes? See lecture 23 pdf pg. 9. As discussed by Dr. Greenspan, two kinds of explanations are possible: 1. Conclusions of individual association (mapping) studies were just wrong somehow 2. There are multiple genetic causes of schizophrenia - mutations or combinations of mutations responsible for schizophrenia in some families are different from those responsible for schizophrenia in other families. In other words, there may simply be no common genetic basis for this complex disease, even though it is highly heritable. 3. How were transgenic mice employed in the study by Young et al. (Nature, 1999) to investigate the role of the vasopressin receptor in controlling the difference between behavioral traits of prarie vs. montane voles, and what were the results of that analysis? See lecture 23 pdf pg. 15-19: The vasopressin receptor (Avpr1a) allele from monogamous prarie voles (which is expressed in a different pattern in the brain compared to the allele from polygamous montane voles) was introduced into the mouse genome. The transgene was expressed in mouse brains in a similar pattern to that seen for the prarie vole gene in prairie vole brains. When treated with vasopressin, these transgenic mice exhibited a higher degree of “affiliative behavior” – a measure of monogamy. This provided evidence that the Avpr1a gene is at least partially responsible for the behavioral differences between prarie and montane voles. 4. The graph below was published as part of the Caspi et al. study (Science, 2003) discussed by Dr. Greenspan
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2008problemset10%20key - ProblemSet#10KEY(BICD100W08 1...

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