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KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE110475 | GEO | 2018/02/12

REPOSITORIES: GEO

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KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis.

Project description:Epithelial tissues rely on a highly coordinated balance between self-renewal, proliferation, and differentiation, disruption of which may drive carcinogenesis. The epigenetic regulator KMT2D (MLL4) is one of the most frequently mutated genes in all cancers, particularly epithelial cancers, yet its normal function in these tissues is unknown. Here, we identify a novel role for KMT2D in coordinating this fine balance, as depletion of KMT2D from undifferentiated epidermal keratinocytes results in reduced proliferation, premature spurious activation of terminal differentiation genes, and disorganized epidermal stratification. Genome-wide, KMT2D interacts with p63 and is enriched at its target enhancers. Depletion of KMT2D results in a broad loss of enhancer histone modifications H3 Lys 4 (H3K4) monomethylation (H3K4me1) and H3K27 acetylation (H3K27ac) as well as reduced expression of p63 target genes, including key genes involved in epithelial development and adhesion. Together, these results reveal a critical role for KMT2D in the control of epithelial enhancers and p63 target gene expression, including the requirement of KMT2D for the maintenance of epithelial progenitor gene expression and the coordination of proper terminal differentiation.

| S-EPMC5830930 | biostudies-literature

KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis [RNA-Seq]

Project description:KMT2D plays a critical role in the control of epithelial enhancers and p63 target gene expression, including the re-quirement of KMT2D for the maintenance of epithelial progenitor gene expression and the coordination of proper terminal differentiation.

2018-02-12 | GSE110467 | GEO

KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis [ChIP-Seq]

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KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis

Project description:KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis

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KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis [ChIP-Seq]

Project description:KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis [ChIP-Seq]

| PRJNA433767 | ENA

KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis [RNA-Seq]

Project description:KMT2D regulates p63 target enhancers to coordinate epithelial homeostasis [RNA-Seq]

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Transcription factor p63 bookmarks genomic loci in epithelial cells and regulates a subset of target genes during epidermal differentiation through dynamic enhancers

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-05-01 | E-GEOD-59827 | biostudies-arrayexpress

Transcription factor p63 bookmarks genomic loci in epithelial cells and regulates a subset of target genes during epidermal differentiation through dynamic enhancers

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-05-01 | GSE59827 | GEO

p63 establishes epithelial enhancers at critical craniofacial development genes.

Project description:The transcription factor p63 is a key mediator of epidermal development. Point mutations in p63 in patients lead to developmental defects, including orofacial clefting. To date, knowledge on how pivotal the role of p63 is in human craniofacial development is limited. Using an inducible transdifferentiation model, combined with epigenomic sequencing and multicohort meta-analysis of genome-wide association studies data, we show that p63 establishes enhancers at craniofacial development genes to modulate their transcription. Disease-specific substitution mutation in the DNA binding domain or sterile alpha motif protein interaction domain of p63, respectively, eliminates or reduces establishment of these enhancers. We show that enhancers established by p63 are highly enriched for single-nucleotide polymorphisms associated with nonsyndromic cleft lip ± cleft palate (CL/P). These orthogonal approaches indicate a strong molecular link between p63 enhancer function and CL/P, illuminating molecular mechanisms underlying this developmental defect and revealing vital regulatory elements and new candidate causative genes.

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p63 establishes epithelial enhancers de novo at critical craniofacial development genes

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-02-15 | GSE126417 | GEO