If I remember correctly we were taught (in CON663) human X inactivation is random, whereas in mouse, X inactivation occurs on the paternally derived X chromosome. Is this wrong (am I wrong)? How do the authors simulate this "human" (random) model?
- It is thought that the X paternal (Xp) inactivation may occur though a resistance imprint on the X maternal (Xm); this imprint inhibits Xm from being inactivated. Thus paternal Xist leads to silencing of Xp.
- "The paternal X chromosome is initially inactivated in all cells of cleavage-stage embryos and then selectively reactivated in the subset of cells that will form the embryo, with random X inactivation occurring thereafter."
- After the blastocyst is formed the Inner cell mass (ICM) looses the Xp Xist RNA coating and histone modifications and Xp is reactivated, followed by random X inactivation.
- Why do you think this process occurs? What is the evolutionary advantage?
- Perhaps an artifact of evolution?
- A carryover effect from MSCI (silencing of X&Y in male germ line -sperm cells).
- Heard E. Recent advances in X-chromosome inactivation. Curr Opin Cell Biol. 2004 Jun;16(3):247-55. DOI:10.1016/j.ceb.2004.03.005 |
Why is dosage compensation important? What genes are on the X chromosome that cause problems when you have gene duplication?
- How do Chaumeil, et al., track a "single species" of mRNA transcripts?
- How to they demonstrate the absence of transcription? What is a major drawback to this method? Do they truly demonstrate "absence of transcription?"
--Chris 22:22, 23 April 2007 (EDT)
Q1. How do you think the Xist transcript is able to exclude RNA Pol II and other transcription components from a "defined" region? How would you go about testing your hypothesis?
Q2. In relation to Q1 - what do you think the Xist domain is comprised of?
- What approach do the authors take in order to resolve the apparent contradition of early exclusion of transcription machinery within 1-2 days and other reports showing that X-linked gene repression only begins after 2 days of differentiation?
- What possible role(s) might the jarid1c gene play that would excuse it from full inactivation?