Polycomb Group-Mediated Gene Silencing Mechanisms: Stability Versus Flexibility

Abstract

Polycomb group (PcG) proteins are highly conserved chromatin factors that repress transcription of particular target genes in animals and plants. PcG proteins form multimeric complexes that act on their target genes through the regulation of post-translational histone modifications, the modulation of chromatin structure and chromosome organization. PcG proteins have long been considered as a cellular memory system that stably locks regulatory chromatin states for the whole lifespan of the organism. However, recent work on the genome-wide distribution of PcG components and their associated chromatin marks in vertebrate cells and Drosophila have challenged this view, revealing that PcG proteins confer dynamic transcriptional control of key developmental genes during cell differentiation and development.

KEYWORDS::

• chromatin marks
• chromatin structure
• development
• differentiation
• embryonic stem cells
• epigenetic regulation
• genome-wide mapping
• nuclear organization
• pluripotency
• Polycomb group complexes

Author note

In a recent paper, Margueron et al. add an important insight into the mechanism of inheritance of the PcG-dependent chromatin marks[140]. They show that EED, a PRC2 component, specifically binds to histone tails carrying trimethyl-lysine residues such as H3K27me3, leading to the stimulation of the methyltransferase activity of PRC2. This work suggests a model for the propagation of silent chromatin states through DNA replication.

Acknowledgements

We thank Bernd Schuettengruber, Tom Sexton and Thierry Cheutin for helpful discussions and for critical readings of the manuscript. We apologize to those whose recent publications we were unable to quote due to space limitations.

Financial & competing interests disclosure

The authors are members of the Giacomo Cavalli laboratory and are supported by the CNRS, the Agence Nationale de la Recherche, and the Association pour la Recherche sur le Cancer. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The authors are members of the Giacomo Cavalli laboratory and are supported by the CNRS, the Agence Nationale de la Recherche, and the Association pour la Recherche sur le Cancer. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.