7.342:Discussion

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==[[7.342: Week 1 Questions|Week 1: Introduction]]==
==[[7.342: Week 1 Questions|Week 1: Introduction]]==
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==[[7.342: Week 2 Questions|Week 2: Chromatin Functions to Define Cell State]]==
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==[[7.342: Week 2 Questions|Week 2: Chromatin functions to define cell state]]==
==[[7.342: Week 3 Questions|Week 3: Chromatin structure and discovery of chromatin modifying enzymes]]==
==[[7.342: Week 3 Questions|Week 3: Chromatin structure and discovery of chromatin modifying enzymes]]==
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==[[7.342: Week 4 Questions|Week 4: Methylation and the histone code]]==
==[[7.342: Week 4 Questions|Week 4: Methylation and the histone code]]==
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Lachner et al:
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==[[7.342: Week 5 Questions|Week 5: Heritable gene expression]]==
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Presumably the authors of this paper are short of time. It would have been nice if they'd replicated some of the studies shown in the second paper; including perhaps a loss of function analysis in a model organism.
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Wysocka et al:
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Figure 5D shows an increase in the levels of dimethylated K4 in HOXA9, when WDR5 is knocked down, using WDR5 siRNA. The authors say this data is reproducible; but it doesn't seem to be explained by their model.
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- Manpreet
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Wysocka et al.
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I think the increase in DiMeK4 in HOXA9 P2 can be explained by the decrease in trimethylation, e.g. less DiMeK4 is converted to TriMeK4, that's why the levels go up; which fits the model; moreover they see the same in HOXC8 P4; but in HOXC8 P3 the levels go down which can not be explained at all, I think. Maybe if they had more WDR5 targets the results would me more consistent. They say there might be differences in the dynamic of regulation between the two Hox genes anyway
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Lachner et al.
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In the WDR5 paper they do ChIP and gene expression analysis. Maybe they might have done it for the HP1 paper too, if, of course it was possible to do in 2001 (which I don't know). Also, is there any reason for using (Myc)3-tagging other than just not having specific anibodies against the proteins of interest?
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Georgi
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Lachner et al.
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What does it mean to "mock-infect" the fibroblasts during the experiment to look for nuclear localization of SUV39H1 proteins?
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Wysocka el at.
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When the authors look for defects from knockdown of xWDR5, they use use embryos derived from eggs of multiple frogs so that there will not be phenotypic differences from different genetic backgrounds. How does using eggs from many frogs do this? It seems like they would want to use embryos from the same frog instead.
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~Amber
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Wysocka et al
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They suggest that their data provides evidence that WDR5 acts as a "sensor" protein - in what way? It does not seem to show how the timing of WDR5 binding and subsequent activation is related to signals that indicate expression would be appropriate (although it does show that WDR5 would be a good target for manipulating/ regulating expression)
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Lachner et al
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This paper discusses what features of HP1 are required for it to bind the H3 lys 9 N terminus. However the experiments only show the characteristics needed in vitro - I think they should have done the pull down assay with nucleosomes. Also, what is the significance of understanding the binding? Why would dimerization be important and do these results actually show that it is necessary?
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-Holly
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==[[7.342: Week 6 Questions|Week 6: Pluripotency regulators and stem cell differentiation]]==
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Wysocha et al
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==[[7.342: Week 7 Questions|Week 7: Regulation of Early Development by Polycomb Proteins]]==
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I found their suggestion that WDR5 specifically recognizes the H3 tail methylated at K4 a bit confusing, and do not understand how they made that leap from the analysis of Ash2 and RbBP5.
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==[[7.342: Week 8 Questions|Week 8: Master Regulators of Differentiation: The Story of MyoD]]==
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Lachner et al
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==[[7.342: Week 9 Questions|Week 9: Transdifferentiation, Dedifferentiation, and the Adoption of Alternate Cell Fates]]==
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I really enjoyed how they used the GFP analysis to better show that HP1 localization is dependent on Suv39h activity and not Suv39h proteins, and the result of 80-90% was so high. I would however, have liked to hear more about how Lys9 in H3 acts like a molecular switch, because I think that is one of the strongest suggestions in their paper.
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==[[7.342: Week 10 Questions|Week 10: The RNAi machinery and chromatin modifications]]==
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Elizabeth
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==[[7.342: Week 11 Questions|Week 11: Chromatin Misregulation in Cancer]]==
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Current revision

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

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

Contents

Week 1: Introduction

Week 2: Chromatin functions to define cell state

Week 3: Chromatin structure and discovery of chromatin modifying enzymes

Week 4: Methylation and the histone code

Week 5: Heritable gene expression

Week 6: Pluripotency regulators and stem cell differentiation

Week 7: Regulation of Early Development by Polycomb Proteins

Week 8: Master Regulators of Differentiation: The Story of MyoD

Week 9: Transdifferentiation, Dedifferentiation, and the Adoption of Alternate Cell Fates

Week 10: The RNAi machinery and chromatin modifications

Week 11: Chromatin Misregulation in Cancer

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