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mSWI/SNF promotes Polycomb repression both directly and through genome-wide redistribution.

Christopher M Weber1,2, Antonina Hafner2, Jacob G Kirkland1,2,3

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The BAF complex antagonizes Polycomb repression but also promotes it in certain cells. Rapid BAF depletion causes Polycomb complexes to shift, altering gene expression and revealing BAF

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Area of Science:

  • Epigenetics and Gene Regulation
  • Chromatin Remodeling
  • Stem Cell Biology

Background:

  • The SWI/SNF (BAF) complex antagonizes Polycomb-mediated repression.
  • BAF also paradoxically promotes Polycomb repression in stem cells and cancer.
  • The dual role of BAF in Polycomb repression is mechanistically unclear.

Purpose of the Study:

  • To investigate the dynamic interplay between the BAF complex and Polycomb repressive complexes (PRCs).
  • To elucidate how BAF influences Polycomb localization and function in mouse embryonic stem cells.
  • To understand the mechanisms underlying BAF's opposing roles in Polycomb-mediated gene silencing.

Main Methods:

  • Utilized targeted protein degradation to rapidly deplete the BAF complex in mouse embryonic stem cells.
  • Analyzed the redistribution of Polycomb repressive complexes PRC1 and PRC2 upon BAF depletion.
  • Assessed changes in chromatin accessibility, epigenomic features, and gene expression.

Main Results:

  • Rapid BAF depletion caused PRC1 and PRC2 to move from highly occupied sites (e.g., Hox clusters) to weakly occupied sites.
  • This redistribution led to decompaction of repressed domains, gain of active epigenomic marks, and transcriptional derepression.
  • Dose-dependent degradation of PRC1 and PRC2 revealed a conventional role for BAF in Polycomb repression, distinct from global redistribution.

Conclusions:

  • BAF complex depletion induces a rapid redistribution of Polycomb repressive complexes, impacting chromatin state and gene expression.
  • BAF plays a dual role: antagonizing Polycomb at some sites while conventionally promoting repression at others.
  • These findings offer new mechanistic insights into the dynamic Polycomb-Trithorax axis regulation in stem cells.