PRC2 is high maintenance
- Jia-Ray Yu1,2,5,
- Chul-Hwan Lee1,2,5,
- Ozgur Oksuz1,2,3,5,
- James M. Stafford1,2,4 and
- Danny Reinberg1,2
- 1Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA;
- 2Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA
- Corresponding author: danny.reinberg@nyulangone.org
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↵5 These authors contributed equally to this work.
Abstract
As the process that silences gene expression ensues during development, the stage is set for the activity of Polycomb-repressive complex 2 (PRC2) to maintain these repressed gene profiles. PRC2 catalyzes a specific histone posttranslational modification (hPTM) that fosters chromatin compaction. PRC2 also facilitates the inheritance of this hPTM through its self-contained “write and read” activities, key to preserving cellular identity during cell division. As these changes in gene expression occur without changes in DNA sequence and are inherited, the process is epigenetic in scope. Mutants of mammalian PRC2 or of its histone substrate contribute to the cancer process and other diseases, and research into these aberrant pathways is yielding viable candidates for therapeutic _targeting. The effectiveness of PRC2 hinges on its being recruited to the proper chromatin sites; however, resolving the determinants to this process in the mammalian case was not straightforward and thus piqued the interest of many in the field. Here, we chronicle the latest advances toward exposing mammalian PRC2 and its high maintenance.
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Article published online ahead of print. Article and publication date are online at http://www.genesdev.org/cgi/doi/10.1101/gad.325050.119.
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