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Transcription factor-dependent ‘anti-repressive’ mammalian enhancers exclude H3K27me3 from extended genomic domains

ABSTRACT: To define and assess the role of transcription factor binding at villus enhancers, we performed ATAC-seq and ChIP-seq. We used RNA-sequencing to profile gene expression changes upon transcription factor loss. Loss of gene expression correlated with transcription factor-dependent enhancers and reveal the role of certain enhancers in H3K27me3 exclusion.

ORGANISM(S): Mus musculus

PROVIDER: GSE98724 | GEO | 2018/01/11

SECONDARY ACCESSION(S): PRJNA386029

REPOSITORIES: GEO

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Transcription factor-dependent 'anti-repressive' mammalian enhancers exclude H3K27me3 from extended genomic domains.

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Mutant p63 affects epidermal cell identity through rewiring the enhancer landscape

Project description:<p>Transcription factor p63 is a key regulator of epidermal keratinocyte proliferation and differentiation. Mutations in the p63 DNA-binding domain are associated with Ectrodactyly Ectodermal Dysplasia Cleft Lip/Palate (EEC) syndrome. Underlying molecular mechanism of these mutations however remain unclear. Here we characterized the transcriptome and epigenome of p63 mutant keratinocytes derived from EEC patients. The transcriptome of p63 mutant keratinocytes deviated from the normal epidermal cell identity. Epigenomic analyses showed an altered enhancer landscape in p63 mutant keratinocytes contributed by loss of p63-bound active enhancers and by unexpected gain of enhancers. The gained enhancers were frequently bound by deregulated transcription factors such as RUNX1. Reversing RUNX1 overexpression partially rescued deregulated gene expression and the altered enhancer landscape. Our findings identify an unreported disease mechanism whereby mutant p63 rewires the enhancer landscape and affects epidermal cell identity, consolidating the pivotal role of p63 in controlling the enhancer landscape of epidermal keratinocytes.</p>

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Replicational dilution of H3K27me3 in mammalian cells and the role of poised promoters

Project description:Differential effect of PRC2 loss on gene repression in intestinal stem cells, transit amplifying cells, and differentiated villus cells in intestine is explained by disparity in the rate of cell division and resulting difference in H3K27me3 loss.

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Mediator complex interaction partners organize the transcriptional network that defines neural stem cells

Project description:Mediator complex regulates transcription by connecting enhancers to promoters. High Mediator binding density defines super enhancers, which regulate cell-identity genes and oncogenes. Protein interactions of Mediator may explain its role in these processes but have not been identified comprehensively. Here we purify Mediator from neural stem cells (NSCs) and identify 75 protein-protein interaction partners. We identify super enhancers in NSCs and show that Mediator-interacting chromatin modifiers colocalise with Mediator at enhancers and super enhancers. Transcription factor families with high affinity for Mediator dominate enhancers and super enhancers and can explain genome-wide Mediator localization. We identify E-box transcription factor Tcf4 as a key regulator of NSCs. Tcf4 interacts with Mediator, colocalises with Mediator at super enhancers and regulates neurogenic transcription factor genes with super enhancers and broad H3K4me3 domains. Our data suggest that high binding-affinity for Mediator is an important organizing feature in the transcriptional network that determines NSC identity.

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A phase separated active subnuclear compartment safeguards repressive chromatin domains [iCLIP]

Project description:The nucleus is composed of membrane-less subnuclear compartments, containing intrinsically disordered proteins and RNAs that phase separate (PS) and contribute to specific nuclear reactions. However, whether and how different subnuclear compartments can intercommunicate remains elusive. Here we identified nuclear bodies with PS features composed of BAZ2A, a factor associating with active chromatin. BAZ2A-bodies depend on active transcription, RNAs, and the non-disordered BAZ2A RNA-binding TAM domain. Although BAZ2A and H3K27me3 occupancies anticorrelate in the linear genome, in the nuclear space BAZ2A-bodies contact H3K27me3-bodies. Disruption of BAZ2A-bodies promotes BAZ2A invasion into H3K27me3-domains, causing H3K27me3-bodies loss, H3K27me3 decrease, and gene upregulation. BAZ2A-bodies formation is negatively regulated by the nuclear-speckles associated lncRNA Malat1 that interacts with BAZ2A and mediates BAZ2A association to chromatin at nuclear speckles, which do not contact BAZ2A-bodies. The results unravel how active compartments protect repressive compartments using PS mechanisms that are promoted or impaired according to the type of RNA interactions with RNA-binding proteins.

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A phase separated active subnuclear compartment safeguards repressive chromatin domains [TSA-seq]

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A phase separated active subnuclear compartment safeguards repressive chromatin domains [ChIP-seq]

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A phase separated active subnuclear compartment safeguards repressive chromatin domains [RNA-seq]

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