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Expression regulation by Pcgf1 in mouse embryonic stem cells

ABSTRACT: The Polycomb repressive complex 1 (PRC1) is essential for fate decisions of embryonic stem (ES) cells. Emerging evidence suggests that six major variants of PRC1 complex, defined by the mutually exclusive presence of Pcgf subunit, regulate distinct biological processes, yet very little is known about the mechanism by which each version of PRC1 instructs and maintains cell fate. Here, we disrupted the Pcgf1, also known as Nspc1 and one of six Pcgf paralogs, in mouse ES cells by the CRISPR/Cas9 technology. We showed that although these mutant cells were viable and retained normal self-renewal, they displayed severe defects in differentiation in vitro. To gain a better understanding of the role of Pcgf1 in transcriptional control of differentiation, we analysed mRNA profiles from Pcgf1 deficient cells using RNA-seq. In contrast to the canonical role of PRC1 in gene repression, we found that Pcgf1 mainly functioned as a transcriptional activator to drive expression of many genes involved in ectoderm and mesoderm differentiation. Chromatin immunoprecipitation experiments demonstrated that Pcgf1 deletion caused a decrease in Ring1B and its associated H2AK119ub1 mark binding to target genes. Altogether, our results revealed an unexpected function of Pcgf1 in gene activation during ES cell maintenance.

ORGANISM(S): Mus musculus

PROVIDER: GSE95383 | GEO | 2017/06/13

REPOSITORIES: GEO

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