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ChIP-seq profile in in vitro produced mouse morula stage embryos treated with siRNA targeting Pcgf5

ABSTRACT: We obtained H3K27me3 profiles in mouse morula stage embryos (72 h post-insemination (hpi)) which had been in vitro treated with siRNA targeting Pcgf5 from one-cell stage (3 hpi).

ORGANISM(S): Mus musculus

PROVIDER: GSE280946 | GEO | 2024/11/07

REPOSITORIES: GEO

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Transcriptomic profile in in vitro produced mouse morula stage embryos treated with siRNA targeting Pwp1

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Essential role of METTL3 in mitochondrial function and epigenetic regulation during preimplantation development in mice

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ChIP-seq profile in in vitro produced mouse morula stage embryos treated with siRNA targeting Pcgf5

Project description:ChIP-seq profile in in vitro produced mouse morula stage embryos treated with siRNA targeting Pcgf5

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Role of visfatin (Nampt) on early embryogenesis in normal weight and obese mice. Studies on siRNA induced knockdown model.

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Genome-wide H3K27me3 profile in in vitro produced bovine morula treated with MAT2A inhibitor

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Transcriptomic profile in in vitro produced mouse morula stage embryos treated with siRNA targeting Pwp1

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PCGF5 is required for neural differentiation of embryonic stem cells [ChIP-seq]

Project description:Polycomb-group proteins are key regulators of the transcriptional programs that maintain stem cell identity and dictate lineage specification. Polycomb repressor complex 1 (PRC1) contains the E3 ligases RING1A/B, which monoubiquitinate lysine 119 at histone H2A (H2AK119ub1) to regulate gene expression. PRC1 has been sub-classified into six major complexes based on the presence of a PCGF subunit. Here, we find that Pcgf5, one of six PCGF paralogs, is an important requirement in the differentiation of mouse embryonic stem cells (mESCs) towards a neural cell fate. Although PCGF5 is not required for mESC self-renewal, its loss blocks mESC neural differentiation by activating the SMAD2/TGF-β signaling pathway. Inhibition of SMAD2/TGF-β signaling or rescue by overexpression of Pcgf5 can restore the capability of mESCs to differentiate towards a neural cell fate. PCGF5 works by stimulating RING1B-dependent H2AK119ub1 both in vitro and in vivo, leading to the suppression of TGF-β signaling genes. PCGF5 loss-of-function prevents the reduction of H2AK119ub1 and H3K27me3 around neural specific genes and keeps them repressed. Our results showed that PCGF5 might function as both a repressor for SMAD2/TGF-β signaling pathway and a facilitator for neural differentiation. Together, our findings reveal a critical context-specific function for PCGF5 in directing PRC1 to control cell fate.

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MERVL-driven Pcgf5 plays a critical role in the suppression of zygotic genome activation in preimplantation embryos

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RNA-seq of PCGF5 knockout and PCGF3/5 double knockout mouse embryonics stem cells bearing doxycycline-inducible Xist transgene on chromosome 16

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2018-04-04 | E-MTAB-5642 | biostudies-arrayexpress

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