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Interdependence of PRC1 and PRC2 for recruitment to Polycomb Response Elements

Tatyana G Kahn1, Eshagh Dorafshan1, Dorothea Schultheis2

  • 1Department of Molecular Biology, Umeå University, Umeå, 901 87, Sweden.

Nucleic Acids Research
|August 26, 2016
PubMed

Insights

Polycomb Group (PcG) complexes target Polycomb Response Elements (PREs) independently of H3K27me3 or H2AK118ub. PRC1 can bind PREs alone, while PRC2 often requires PRC1 for targeting, changing understanding of PcG repression.

Area of Science:

  • Epigenetics
  • Developmental Biology
  • Molecular Biology

Background:

  • Polycomb Group (PcG) proteins are crucial epigenetic repressors for development and cell differentiation.
  • PcG proteins function through complexes like PRC1 and PRC2, which are essential for gene silencing.
  • The precise targeting mechanisms of PRC1 and PRC2 to Polycomb Response Elements (PREs) remain incompletely understood, with hierarchical models involving histone modifications proposed.

Purpose of the Study:

  • To rigorously test the hypothesis that histone modifications, specifically H3K27me3 and H2AK118ub, are required for targeting Polycomb Group complexes to PREs.
  • To elucidate the roles of PRC1 and PRC2 in targeting PcG complexes to PREs and their interdependence.
  • To investigate the function of H3K27me3 and H2AK118ub in the context of PcG-mediated repression.

Main Methods:

  • Utilized the Drosophila melanogaster model system for precise genetic manipulation and analysis.
  • Performed experiments to assess the binding of PRC1 and PRC2 to PREs in the absence of specific histone modifications (H3K27me3 and H2AK118ub).
  • Investigated the requirement of PRC1 for PRC2 targeting and vice versa.

Main Results:

  • Demonstrated that neither H3K27me3 nor H2AK118ub is necessary for the initial targeting of PRC1 and PRC2 to PREs.
  • Showed that PRC1 can bind to PREs independently of PRC2.
  • Found that PRC2 targeting to many PREs requires the prior presence of PRC1.
  • Revealed that H3K27me3 facilitates the interaction of anchored PcG complexes with surrounding chromatin.
  • Indicated that the majority of H2AK118ub is not directly involved in PcG repression.

Conclusions:

  • The targeting of PcG complexes to PREs is largely independent of H3K27me3 and H2AK118ub.
  • PRC1 and PRC2 exhibit a complex interdependence in targeting, with PRC1 often preceding PRC2.
  • H3K27me3 plays a role in modulating the interaction of PcG complexes with chromatin, rather than initial targeting.
  • H2AK118ub appears largely unrelated to the core PcG repression mechanism at PREs.
  • These findings challenge existing models and suggest novel communication pathways between PRC1 and PRC2 independent of canonical histone marks.

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