Christopher Weber

@chmweber

Stanford postdoc studying chromatin and gene regulation.

San Francisco, CA
Vrijeme pridruživanja: listopad 2010.

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  1. Prikvačeni tweet
    31. sij

    I am excited to share my latest work on ! Here we try to understand how the mSWI/SNF, or the BAF complex, promotes polycomb-mediated repression? 1/n

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  2. proslijedio/la je Tweet
    2. velj
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  3. 31. sij

    I should give a shoutout to and colleagues here for sharing dTAG ligand before it was commercially available and for developing a degron approach that is unbelievably efficient and dosage-sensitive. dTAG is the gold-standard!

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  4. proslijedio/la je Tweet
    31. sij
    Odgovor korisnicima

    Dark side of genetics are indirect effects and global effects through altered distribution. This is great study!

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  5. 31. sij

    Collectively, our data supports the model that BAF activity promotes distal repression by titrating polycomb dosage. We’re sending this out soon, so please let me know if you have any comments, suggestions, or criticism! Thanks for following along! 10/n

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  6. 31. sij

    Finally, if our model is correct then polycomb overexpression should block Hox derepression when Brg1 is degraded. We overexpressed a minimal vPRC1 complex (most catalytic activity) and indeed find that it suppressed derepression! 9/n

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  7. 31. sij

    Is BAF controlling polycomb dosage? We made dTAG mESCs to degrade PRC1, PRC2, and both. We titrate polycomb protein dosage at the same time-point as our Brg1 degron. Voila, we find that intermediate degradation mirrors Brg1 derepression, but maximal is stronger! 8/n

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  8. 31. sij

    We next looked at features associated with active chromatin (K4me3, K27ac, and ATAC) and find that they negatively correlated with polycomb changes. BAF doesn’t generate accessibility to load polycomb and is excluded from repressed domains. BAF isn't working bidirectionally. 7/n

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  9. 31. sij

    Is this loss sufficient to decompact Hox clusters? We collaborated with the Boettiger lab to trace the DNA paths at HoxA and HoxD clusters with ORCA. Indeed, the polycomb loss is actually sufficient to physically decompact Hox! 6/n

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  10. 31. sij

    PRC1 and PRC2 are redistributed from highly bound domains to weakly bound sites genome-wide, consistent with driving the transcriptional response. 5/n

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  11. 31. sij

    Brg1 degradation rapidly derepresses many highly polycomb-bound genes in a time-dependent manner, such as Hox clusters and neurodevelopmental genes. So what happens to polycomb? 4/n

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  12. 31. sij

    Traditional approaches (i.e. cKO/RNAi) take days to deplete proteins and cannot distinguish primary from secondary effects. To address this question directly, we created an mESC line where the ATPase subunit Brg1 can be rapidly degraded (T1/2 ~30m, near-complete ~2h). 3/n

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  13. 31. sij

    BAF directly antagonizes polycomb-mediated repression from flies to humans (i.e. Trithorax Group). Yet, BAF somehow also promotes polycomb-mediated repression. How can BAF do both things? What’s the mechanism? 2/n

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  14. proslijedio/la je Tweet
    18. sij

    Cool new study on how subunit switching of a chromatin remodeler controls neural cell fate! Great things come from and collaborations!

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  15. 15. sij
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  16. 11. sij

    I stumbled upon several fun interviews from scientists that I really look up to. 👏🏻 84th CSHL Symposium: RNA CONTROL & REGULATION via

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  17. 10. sij

    Anyone know why access to NCBI is restricted off-campus, but VPN works?

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  18. proslijedio/la je Tweet
    12. pro 2019.

    Our preprint on splicing dynamics in human cells is now published with 5x more data! Congratulations to Heather and Karine! All data are here: and all analysis scripts are deposited:

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  19. 3. pro 2019.
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  20. 27. stu 2019.

    I’ve known Stephen for a long time. Superb mentor and lab. Seize the opportunity!

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