Ring1B and Suv39h1 delineate distinct chromatin states at bivalent genes during early mouse lineage commitment | Zendy

Olivia Alder | Zendy; Fabrice Lavial | Zendy; Anne Helness | Zendy; Emily Brookes | Zendy; Sandra Pinho | Zendy; Anil Chandrashekran | Zendy; Philippe Arnaúd | Zendy; Ana Pombo | Zendy; Laura P. O’Neill | Zendy; Véronique Azuara | Zendy

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Ring1B and Suv39h1 delineate distinct chromatin states at bivalent genes during early mouse lineage commitment

Author(s) -

Olivia Alder,

Fabrice Lavial,

Anne Helness,

Emily Brookes,

Sandra Pinho,

Anil Chandrashekran,

Philippe Arnaúd,

Ana Pombo,

Laura P. O’Neill,

Véronique Azuara

Publication year - 2010

Publication title -

development

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.754

H-Index - 325

eISSN - 1477-9129

pISSN - 0950-1991

DOI - 10.1242/dev.048363

Subject(s) - biology , chromatin , bivalent chromatin , embryonic stem cell , bivalent (engine) , microbiology and biotechnology , genetics , somatic cell , inner cell mass , induced pluripotent stem cell , epigenetics , blastocyst , gene , embryogenesis , chromatin remodeling , chemistry , organic chemistry , metal

Pluripotent cells develop within the inner cell mass of blastocysts, a mosaic of cells surrounded by an extra-embryonic layer, the trophectoderm. We show that a set of somatic lineage regulators (including Hox, Gata and Sox factors) that carry bivalent chromatin enriched in H3K27me3 and H3K4me2 are selectively targeted by Suv39h1-mediated H3K9me3 and de novo DNA methylation in extra-embryonic versus embryonic (pluripotent) lineages, as assessed both in blastocyst-derived stem cells and in vivo. This stably repressed state is linked with a loss of gene priming for transcription through the exclusion of PRC1 (Ring1B) and RNA polymerase II complexes at bivalent, lineage-inappropriate genes upon trophoblast lineage commitment. Collectively, our results suggest a mutually exclusive role for Ring1B and Suv39h1 in regulating distinct chromatin states at key developmental genes and propose a novel mechanism by which lineage specification can be reinforced during early development.

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