7.342: Week 7 Questions

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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.


Cao et al

In figure 4A there are numbers below each lane that they call 'quantified signals relative to inputs'. Are they just assigning a number to how strong each band appears?

Bracken et al

What is the significance of the sementation repressors they mention in Figure 5Aii?


Cao et al

Could we perhaps have a short review of PcG proteins and the PRC1? Thank you!!

Bracken et al

How do you successful interpret the “Ratio bound/input” graphs in Figure 2b and 3b. The graphs look significant, but how do you interpret them? and why are they necessarily needed in Figure 2 if the information is also displayed in A and C?


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?


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?


Cao: With all these types of modifications that histones can undergo, it seems that the histone code is extremely complicated. Has any type of "histone code map" been developed?

Bracken: These "genome-wide" type of papers are really difficult to read. The conclusion always seems to be along the lines of everything effects everything. In reality, how practical/useful are these types of papers?


Cao et al: In fig. 4A, there is a lot of binding seen of PC to the unmodified peptide. I thought the chromodomain bound to methyl groups. Is this binding via a secondary binding site, or is the specificity of the chromodomain not that high?

Bracken et al: I'm not sure I understand their conclusion [on page 1133] about PcG target genes being preprogrammed to be repressed upon appropriate cell fate signals. Could you explain this please?


Cao, et al.:

I don't understand how they were able to accurately predict that E(Z) is recruited by an Ultrabithorax Polycomb response element. How do they know what targets ESC-E(Z), but not what targets PRC2 to specific genes?

Bracken, et al.:

I am amazed that the PcG proteins are already bound but somehow 'dormant' before differentiation. Figure 6.e strikes me as a little odd - why do they show two possible outcomes of differentiation, one involving protein X? and one involving protein Y?, that appear to have exactly the same effect?