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YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

ABSTRACT: Polycomb repressive complexes( PRCs) play critical role in cell fate decisions during normal development as well as disease progression through mediate histone modifications such as H3K27me3 and H2AK119ub. How exactly PRCs recruited to chromatin remains to be fully illuminated. Here, we report that YTHDF1, a N6-methyladenine (m6A) RNA reader previously known being mainly cytoplasmic, associates with RNF2, a PRC1 protein that mediates H2AK119ub in human embryonic stem cells (hESCs). Specifically, a portion of YTHDF1 localizes in the nuclei and associates with RNF2/ H2AK119ub on a subset of gene loci related to neural development functions. Knock-down YTHDF1 attenuates H2AK119ub modification on these genes and promotes neural differentiation in hESCs. Our findings provide another non-canonical mechanism of YTHDF1 to participate in PRC1 mediated chromatin modification in hESCs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE204824 | GEO | 2023/12/30

REPOSITORIES: GEO

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YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

Project description:Polycomb repressive complexes( PRCs) play critical role in cell fate decisions during normal development as well as disease progression through mediate histone modifications such as H3K27me3 and H2AK119ub. How exactly PRCs recruited to chromatin remains to be fully illuminated. Here, we report that YTHDF1, a N6-methyladenine (m6A) RNA reader previously known being mainly cytoplasmic, associates with RNF2, a PRC1 protein that mediates H2AK119ub in human embryonic stem cells (hESCs). Specifically, a portion of YTHDF1 localizes in the nuclei and associates with RNF2/ H2AK119ub on a subset of gene loci related to neural development functions. Knock-down YTHDF1 attenuates H2AK119ub modification on these genes and promotes neural differentiation in hESCs. Our findings provide another non-canonical mechanism of YTHDF1 to participate in PRC1 mediated chromatin modification in hESCs.

2023-12-30 | GSE185692 | GEO

YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

Project description:YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

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Polycomb suppresses a female gene regulatory network in Sertoli cells

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Project description:Maged1 inactivation induces insensitivity to cocaine by impairing cocaine-evoked release of dopamine and plasticity in the Nucleus accumbens (NAc). Here we have characterized the chromatin epigenetic and transcriptional alterations associated with chronic cocaine exposure in the paraventricular thalamus (PVT, one of the main regulatory inputs of the Nac) in mice WT or conditional KO for Maged1 activity. At the epigenetic level, we focused on the analysis of the genomic coverages of the histone post-translational modification H2AK119ub (monoubiquitination of Lysine 119 of H2A; H2Aub), a repressive chromatin mark associated to polycomb (PRC1) –mediated gene repression since Maged1 specifically interact with H2A upon cocaine administration and is required for cocaine-induced increase of H2AK119ub levels in the PVT.

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Project description:Polycomb repressive complex 1 (PRC1) comprises two different complexes: CBX-containing canonical PRC1 (cPRC1) and RYBP/YAF2-containing variant PRC1 (vPRC1). RYBP and its paralog YAF2 recruit vPRC1 to catalyze H2AK119ub through a positive-feedback model. Here, we show that expression of RYBP and YAF2 decreases and increases, respectively, during neural differentiation of embryonic stem cells (ESCs). Rybp knockout impairs neural differentiation by activating Wnt signaling and derepressing nonneuroectoderm-associated genes. However, Yaf2 knockout promotes neural differentiation and leads to redistribution of RYBP binding, increases enrichment of RYBP and H2AK119ub on the RYBP-YAF2 co-targeted genes, and prevents ectopic derepression of nonneuroectoderm-associated genes in neural-differentiated cells. Furthermore, the phase separations mediated by RYBP alone or together with RING1B are easier and more stable than those by YAF2, which might facilitate the deposition of H2AK119ub more abundantly by RYBP-PRC1 than YAF2-PRC1. Together, this study reveals that RYBP might maintain repressed chromatin more strongly and function differentially in regulating mESC neural differentiation compared with YAF2.

2023-10-09 | GSE213413 | GEO

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Project description:Polycomb repressive complex 1 (PRC1) comprises two different complexes: CBX-containing canonical PRC1 (cPRC1) and RYBP/YAF2-containing variant PRC1 (vPRC1). RYBP-vPRC1 or YAF2-vPRC1 catalyzes H2AK119ub through a positive-feedback model; however, whether RYBP and YAF2 have different regulatory functions is still unclear. Here, we show that the expression of RYBP and YAF2 decreases and increases, respectively, during neural differentiation of embryonic stem cells (ESCs). Rybp knockout impairs neural differentiation by activating Wnt signaling and derepressing nonneuroectoderm-associated genes. However, Yaf2 knockout promotes neural differentiation and leads to redistribution of RYBP binding, increases enrichment of RYBP and H2AK119ub on the RYBP-YAF2 cotargeted genes, and prevents ectopic derepression of nonneuroectoderm-associated genes in neural-differentiated cells. Taken together, this study reveals that RYBP and YAF2 function differentially in regulating mESC neural differentiation.

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ChIPseq on H3K27ac, H3K27me3 and H2AK119Ub on TXY cell line

Project description:During development, changes in gene transcription are accompanied by changes in chromatin modification but the order and causality of events often remain unclear. Here we address this question using X-chromosome inactivation (XCI), which entails chromosome-wide gene silencing and heterochromatin formation. We initiate XCI in female, mouse embryonic stem cells by inducing Xist expression and monitor subsequent changes in transcription and chromatin modification by allele-specific TTseq and ChIPseq respectively. An unprecedented temporal resolution has enabled us to define early alterations in chromatin that are induced upon Xist RNA coating. Xist-induced repression begins with histone deacetylation, which involves the histone deacetylase HDAC3 and occurs before efficient loss of H3K4me3 and H3K4me1 modifications. Polycomb-associated repressive histone marks accumulate rapidly, starting with PRC1-associated H2AK119Ub and followed by PRC2-associated H3K27me3. However, polycomb accumulates initially at large premarked domains, some of which correspond to Xist entry sites, and then spreads into genes. We also show that spreading can only ensue when transcriptional silencing has occurred. These results establish a detailed epigenomic time course for XCI and reveal a hierarchy of events with chromatin playing an important role in transcriptional silencing of the X chromosome.

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