- What was Mary Lyon's observation about female coat color, and what were the implications of this observation? How does male mouse coat color phenotype differ for these same alleles compared to that of females?
- What in essence was her hypothesis to explain this coat color phenomenon? What additional experiments would you like to see done to test this hypothesis?
- At one point, she writes that there were patches of 1 color or another, but also "patches of intermediate color due to cell mingling in development". What is she talking about here?
- How did her hypothesis fit with cytogenetic observations of the X-chromosome in cells?
- What can you conjecture about the timing of X-inactivation during development in female mice, and whether one allele in preference to the other (maternal or paternally-inherited X-chromosome) becomes affected?
- Since Mary Lyon’s discovery of X-inactivation in mice, two non-coding RNAs, Tsix and Xist, have been shown to participate in X-inactivation. How do these RNAs contribute to X-gene silencing? Do they act in cis or trans?
- Chromosomal aneuploidy (including partial monosomy or trisomy) is generally associated with severe developmental abnormalities and disease. X-inactivation (as it occurs in humans and mouse) is a mechanism for dosage compensation. However, recent work in both mouse and humans suggests that X-inactivation is only part of the story when it comes to X-chromosome dosage compensation, because some genes escape X-inactivation. How is the dosage of these genes regulated? Based upon these new data, what are the mechanisms used to maintain proper dosage compensation in mammals?
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