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Chromatin folding and nuclear architecture: PRC1 function in 3D.

Authors
  • Illingworth, Robert S1
  • 1 MRC Centre for Regenerative Medicine, Institute for Regeneration and Repair, The University of Edinburgh, Edinburgh BioQuarter, 5 Little France Drive, Edinburgh, EH16 4UU, United Kingdom. Electronic address: [email protected] , (France)
Type
Published Article
Journal
Current opinion in genetics & development
Publication Date
Apr 01, 2019
Volume
55
Pages
82–90
Identifiers
DOI: 10.1016/j.gde.2019.06.006
PMID: 31323466
Source
Medline
Language
English
License
Unknown

Abstract

Embryonic development requires the intricate balance between the expansion and specialisation of defined cell types in time and space. The gene expression programmes that underpin this balance are regulated, in part, by modulating the chemical and structural state of chromatin. Polycomb repressive complexes (PRCs), a family of essential developmental regulators, operate at this level to stabilise or perpetuate a repressed but transcriptionally poised chromatin configuration. This dynamic state is required to control the timely initiation of productive gene transcription during embryonic development. The two major PRCs cooperate to target the genome, but it is PRC1 that appears to be the primary effector that controls gene expression. In this review I will discuss recent findings relating to how PRC1 alters chromatin accessibility, folding and global 3D nuclear organisation to control gene transcription. Copyright © 2019 The Author. Published by Elsevier Ltd.. All rights reserved.

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