Journal
MOLECULAR CELL
Volume 70, Issue 3, Pages 435-+Publisher
CELL PRESS
DOI: 10.1016/j.molcel.2018.03.019
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Funding
- NYU Flow Cytometry Core [NIH/NCI P30CA016087]
- Kimmel Scholars Program
- David and Lucile Packard Foundation
- NIH [R01GM115882, NCI R01CA199652]
- Alexander von Humboldt Foundation
- American Cancer Society [PF-17-035-01]
- Swedish Society for Medical Research
- Making Headway Foundation [189290]
- Howard Hughes Medical Institute (HHMI)
- NATIONAL CANCER INSTITUTE [R01CA199652, P30CA016087] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM115882] Funding Source: NIH RePORTER
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The maintenance of gene expression patterns during metazoan development is achieved, in part, by the actions of polycomb repressive complex 2 (PRC2). PRC2 catalyzes mono-, di-, and trimethylation of histone H3 at lysine 27 (H3K27), with H3K27me2/3 being strongly associated with silenced genes. We demonstrate that EZH1 and EZH2, the two mutually exclusive catalytic subunits of PRC2, are differentially activated by various mechanisms. Whereas both PRC2-EZH1 and PRC2-EZH2 are able to catalyze mono- and dimethylation, only PRC2-EZH2 is strongly activated by allosteric modulators and specific chromatin substrates to catalyze trimethylation of H3K27 in mouse embryonic stem cells (mESCs). However, we also show that a PRC2-associated protein, AEBP2, can stimulate the activity of both complexes through a mechanism independent of and additive to allosteric activation. These results have strong implications regarding the cellular requirements for and the accompanying adjustments in PRC2 activity, given the differential expression of EZH1 and EZH2 upon cellular differentiation.
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