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GDCB 510 Questions for Sept 21, 2006 Instructions: please provide short answers (one or two sentences) to the following questions. We will use your answers to discuss the papers in class, although we may not discuss every question. At the end of class I will collect your written answers. If you provide written answers to all of today’s questions, you will receive 2.5 points. There is no other written assignment this week. If you participated in discussion once over the last few lectures, you will receive 2.5 pts. First reading, Research paper: Bultman SJ et al., Maternal BRG1 regulates zygotic genome activation in the mouse. Genes and Development 20 (2006):1744-54 1. What is zygotic genome activation (ZGA)? When does ZGA happen in Drosophila, and when does it happen in the mouse? 2. Consider the statement: “By the very nature of the ZGA process, ZGA must be under maternal control.” Explain why you agree or disagree with this statement. 3. Explain why, for most mutations that have a lethal phenotype, it may never be possible to test whether or not the mutation has a maternal effect. 4. For mutations that are lethal to developing embryos, what can you conclude about the importance of the gene in the adult form of the organism? 5. What is a null mutation? The phenotype of null Brg1 embryos is lethality at the blastocyst (~40-cell) stage. Does this mean that the embryo does not require the BRG protein until it reaches the 40-cell stage? 6. Why has the maternal effect of a Brg1 null mutation not been previously examined? 7. How was Cre-lox used to provide a genetic tool to test the hypothesis of that Brg1 is a maternal effect gene? 8. Brg1Zp3-Cre is a conditional allele, with a conditional mutant phenotype. What are the permissive conditions, and what are the restrictive conditions? 9. If the wild-type activity level of Brg1 is 1 unit, what is the activity level of each of the following alleles: Brg1null, Brg1floxed, Brg1floxed. 10. In Table 1, what strain was Brg1Zp3-Cre crossed to? Which genotype was the male, which was female? What do the data in Table 1 indicate? Are these data alone sufficient to establish a maternal effect function for Brg1? 11. What does Fig 1C show? And what does Fig 1D show? Why are the experiments in Figure 1 important? 12. At the end of page 1746, a paragraph begins “The relevant …” Here the authors consider the data in Figure 2. Are the presented data now sufficient to establish a maternal effect function for Brg1? Which genetic explanations for the ZGA phenotype, do these data eliminate? 13. What is the earliest stage in embryo development (how many cells), when the Brg1 gene is required? Is this consistent with a role for Brg1 in ZGA? Second reading, Research paper: Lolle, SJ, JL Victor, JM Young, and RE Pruitt. "Genome-wide non-mendelian inheritance of extra-genomic information in Arabidopsis." Nature. 434 (2005): 505-509. Comment that accompanied the Lolle et al. publication: Weigel, D, and G Jurgens. "Genetics: hotheaded healer." Nature. 434 (2005): 443. Comments after publication (These papers are optional): * Chaudhury, A. "Plant genetics: hothead healer and extragenomic information." Nature. 437 (2005): E1; discussion E2. * Ray, A. "Plant genetics: RNA cache or genome trash?" Nature. 437 (2005): E1-2; discussion E2. * Comai L and Cartwright RA “A toxic mutator and selection alternative to the non- mendelian, RNA cache hypothesis for hothead reversion.” Plant Cell 17 (2005): 2856-8 Discussion questions: Questions 14 – 20 refer to the initial observation, that hth reverts to HTH: 14. Describe the initial, unusual inheritance patterns seen in hth/hth mutants. We will call this “the hth phenomenon.” Be prepared to explain Table 1 to the class. 15. What fundamental Mendelian principle is violated by the hth phenomenon? 16. Why is it significant that several hth alleles all cause this effect? 17. Explain how the hth phenomenon could be cause by incomplete penetrance. What data argue against a hypothesis of incomplete penetrance? 18. Explain the seed contamination and pollen contamination hypotheses. 19. What data argue against the contamination hypotheses? 20. There are other, conventional explanations that are tested by the authors. They conclude that all of them are poor explanations of the hth phenomenon. Do you disagree with any of these conclusions? 21. Is hth-mediated reversion limited to alleles of the HTH gene, or can it occur in other parts of the genome? If so, then are there limits on the types of changes? Can you think of allele types not examined here, that would be interesting to test? 22. When reversion occurs, is the new (reverted) sequence random, or does it come from a particular pool of alleles? 23. What is the hth mutant phenotype. How might that be relevant to the hth phenomenon, in terms of reproduction? In terms of biochemistry? 24. Many people are still suspicious of contamination in these experiments. Why? Can you suggest a good experiment to test for this?
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