7.342: Week 7 Questions: Difference between revisions

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==Holly==
==Holly==
Cao et al:
Cao et al:
They discuss the effect of E(z) being unable to bind in homozygous    E(z)61 embryos (those reared at 29oC) –what is the effect of increasing the temperature to 29oC when the Drosophila are fully developed (after being reared at 18oC)? Is H3-K27 methylation decreased in this instance? Does the phenotype/ gene expression pattern change? I.e. is the HMTase activity required continuously or only transiently to maintain repression?  
They discuss the effect of E(z) being unable to bind in homozygous    E(z)61 embryos (those reared at 29oC) –what is the effect of increasing the temperature to 29oC when the Drosophila are fully developed (after being reared at 18oC)? Is H3-K27 methylation decreased in this instance? Does the phenotype/ gene expression pattern change? I.e. is the HMTase activity required continuously or only transiently to maintain repression?  



Revision as of 18:39, 25 October 2006

7.342: Reading the Blueprint of Life: Transcription, Stem Cells, & Differentiation

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Post discussion, questions, or comments about the Week 6 course material here.

Amber

Elizabeth

Georgi

Cao et al.

What is the function of methylation of H3-K79 and DOT1?

What is the function of PhoRC?

They propose a model in which PRC1 inhibits SWI/SNF; is it known now how the transcriptional repression works?

Bracken et al.

I think it is really striking that PcGs appear associated with Hox genes without repressing them and repress them afterwards during differentiation. How might this be regulated? Also if there are ~1000 PcG target genes, do they all have PREs? Actually are there PREs in humans, they don’t mention this anywhere and how is recruitment of PcGs regulated?


Holly

Cao et al:

They discuss the effect of E(z) being unable to bind in homozygous E(z)61 embryos (those reared at 29oC) –what is the effect of increasing the temperature to 29oC when the Drosophila are fully developed (after being reared at 18oC)? Is H3-K27 methylation decreased in this instance? Does the phenotype/ gene expression pattern change? I.e. is the HMTase activity required continuously or only transiently to maintain repression?

Bracken et al:

They mention that PcG binding positions on target genes fall in to one of two different catergories – ‘bell curves’ or ‘blanket’ types. What is the functional significance of this? Does it correlate at all with the different proposed mechanisms by which PcGs regulate cell fate?

Kathy

Manpreet

Zak

.