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Gene silencing triggers polycomb repressive complex 2 recruitment to CpG islands genome wide

Eva Madi Riising1, Itys Comet1, Benjamin Leblanc2

  • 1Biotech Research and Innovation Centre (BRIC), University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen, Denmark; Centre for Epigenetics, University of Copenhagen, Ole Maaløes Vej 5, 2200 Copenhagen, Denmark.

Molecular Cell
|July 8, 2014
PubMed

Insights

Polycomb repressive complex 2 (PRC2) is not essential for initiating gene silencing during cell differentiation. Instead, PRC2 binds to untranscribed genes, maintaining their silenced state and protecting cell identity.

Area of Science:

  • Epigenetics and gene regulation
  • Developmental biology
  • Cancer biology

Background:

  • Polycomb group (PcG) proteins are crucial for normal development and frequently altered in cancer.
  • The precise role of PcG proteins in initiating and maintaining gene silencing is not fully understood.

Purpose of the Study:

  • To investigate the role of Polycomb repressive complex 2 (PRC2) in gene silencing during mouse embryonic stem cell differentiation.
  • To determine the factors governing PRC2 binding to target genes.

Main Methods:

  • Gene knockout of PRC2 in mouse embryonic stem cells (mESCs).
  • Analysis of gene expression changes following PRC2 knockout.
  • Genome-wide PRC2 recruitment analysis under conditions of transcriptional inhibition.
  • Chromatin immunoprecipitation and sequencing to analyze PRC2 binding sites.

Main Results:

  • PRC2 knockout did not cause significant gene expression changes in mESCs and was not required for initiating gene silencing during differentiation.
  • Transcriptional inhibition induced genome-wide ectopic PRC2 recruitment to target genes.
  • PRC2 binding is restricted to nucleosome-free CpG islands (CGIs) of untranscribed genes.

Conclusions:

  • Transcriptional state, not PRC2 itself, dictates PRC2 binding.
  • PRC2 likely binds by default to nontranscribed CGI genes to maintain their silenced state and preserve cell identity.

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