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H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [RNA-seq]

ABSTRACT: H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [RNA-seq]

PROVIDER: PRJNA1211021 | ENA |

REPOSITORIES: ENA

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H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [RNA-seq]

Project description:Heterochromatin is a key architectural feature of eukaryotic chromosomes, essential for cell type-specific gene expression and genome stability. In the mammalian nucleus, heterochromatin is segregated from transcriptionally active euchromatic regions (A compartments), forming large, condensed, and inactive nuclear compartments (B compartments). However, the mechanisms underlying its spatial organization remain incompletely understood. Histone H3 lysine 9 and lysine 27 trimethylation (H3K9me3 and H3K27me3) are two major epigenetic modifications that enrich constitutive and facultative heterochromatin, respectively. Previously, we found that the redistribution of H3K27me3 following the loss of H3K9 methylation contributes to heterochromatin maintenance, while the simultaneous loss of both H3K27me3 and H3K9 methylation induces heterochromatin decondensation in mouse embryonic fibroblasts. However, nearly all B compartments were preserved despite the loss of these repressive chromatin modifications. These findings suggest that other factors are responsible for maintaining B compartments under these conditions. In this study, we explored the role of another repressive chromatin modification, PRC1-mediated H2A K119 monoubiquitylation (H2AK119ub/uH2A), in maintaining heterochromatin structure following the loss of H3K9/K27 methylation. We found that uH2A and H3K27me3 independently accumulate in the B compartments after the loss of H3K9 methylation in iMEFs and cooperatively maintain heterochromatin. Our data indicates that the PRC1- uH2A pathway contributes to maintain heterochromatin organization following the loss of H3K9/K27 methylation in mammalian cells.

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H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [ChIP-seq]

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H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [Hi-C]

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H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [ChIP-seq]

Project description:H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [ChIP-seq]

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H3K27me3 and the PRC1-H2AK119ub pathway cooperatively maintain heterochromatin and transcriptional silencing after the loss of H3K9 methylation [Hi-C]

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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.

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YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

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Project description:Identification of BMI1, RYBP and H2AK119UB interactome in Glioblastoma (GBM) to elucidate BMI1 roles independent of the PRC1-complex in GBM.

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YTHDF1 facilitates PRC1 mediated H2AK119ub in Human ES Cells

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