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Mouse ES cells expressing catalytically inactive Ring1B display impaired Ring1B and H3K27me3 deposition.

ABSTRACT: ChIP-seq for H3K27me3 and Ring1B was performed in WT mESCs and mESCs containing catalytically inactive Ring1B (I53A mutant). Cells expressing catalytically inactive Ring1B maintain the spatial distribution of Ring1B and H3K27me3 but at reduced levels. These findings support the notion that PRC2 recruitment is, in part, dependent on H2A ubiquitination (H2AK119ub). Two biological replicates were performed for Ring1B and H3K27me3 ChIPs in WT and Ring1B I53A/I53A mouse ESCs. Input chromatin was sequenced for each replicate as a control for ChIP enrichment.

ORGANISM(S): Mus musculus

SUBMITTER: Robert Illingworth

PROVIDER: E-GEOD-69955 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The E3 ubiquitin ligase activity of RING1B is not essential for early mouse development.

Illingworth Robert S RS Moffat Michael M Mann Abigail R AR Read David D Hunter Chris J CJ Pradeepa Madapura M MM Adams Ian R IR Bickmore Wendy A WA

Genes & development 20150901 18

Polycomb-repressive complex 1 (PRC1) and PRC2 maintain repression at many developmental genes in mouse embryonic stem cells and are required for early development. However, it is still unclear how they are targeted and how they function. We show that the ability of RING1B, a core component of PRC1, to ubiquitinate histone H2A is dispensable for early mouse embryonic development and much of the gene repression activity of PRC1. Our data support a model in which PRC1 and PRC2 reinforce each other' ...[more]

PMID: 26385961

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