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Loss of the C-terminus of p63 leads to an increased expression of extracellular matrix genes in keratinocytes due to a preferential binding of p63 to promoters

ABSTRACT: Loss of the C-terminus of p63 leads to an increased expression of extracellular matrix genes in keratinocytes due to a preferential binding of p63 to promoters

PROVIDER: PRJNA1006762 | ENA |

REPOSITORIES: ENA

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Loss of the C-terminus of p63 leads to an increased binding of p63 to promoters and histone acetylation [ChIP-seq]

Project description:The transcription factor p63 is a master gene of epithelial development. p63 regulates expression of genes related to proliferation, differentiation and adhesion by binding epithelial enhancers. Biochemically, p63 interacts with chromatin via its DNA binding domain, while N-terminus is essential for the fine tuning of its transcriptional activity. However, the role of the C-terminus of p63 remains elusive. Here, we investigate the role of the C-terminal SAM domain of p63 in vivo. We generated Krt14-specific knock-out of the SAM domain (exon 13) of p63 which resulted in expression of the p63b isoform. Most of p63b expressing mice die 2-3 months after birth and show alteration of skin, adipose tissue and muscle morphology. Mechanistically, ChIP-seq analysis showed an increased binding of p63b to gene promoters. Further integration of transcriptome and genome occupancy analyses revealed that p63b binds more readily promoter regions of extracellular matrix (ECM) genes leading to their enhanced expression. Aberrant expression of ECM genes by p63b disrupts normal adhesion of keratinocytes to basal lamina triggering systemic inflammation and premature death. Altogether, our data suggest that C-terminus ensures p63 selectivity in enhancer binding to maintain physiological levels of extracellular matrix and adhesion proteins.

2025-07-22 | GSE241105 | GEO

Loss of the C-terminus of p63 leads to an increased expression of extracellular matrix genes in keratinocytes [RNA-seq]

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Loss of the C-terminus of p63 leads to an increased expression of extracellular matrix genes in keratinocytes due to a preferential binding of p63 to promoters

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Pathway Preferential Estrogens prevent hepatosteatosis due to ovariectomy and high-fat diets

Project description:Pathway Preferential Estrogens prevent hepatosteatosis due to ovariectomy and high-fat diets

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Genome wide identification of p63 binding sites in human neonatal foreskin keratinocytes

Project description:We report here genome wide identification of p63 binding sites in cycling neonatal foreskin keratinocytes using high throughput sequencing of ChIP enriched DNA. Analysis of gene ontology, database mining with integration with publicly available data, reveals a role for p63 in transcriptional regulation of multiple genes genetically linked to cleft palate. In addition, we identify AP-2Î±, a transcription factor which, when mutated, also results in craniofacial clefting syndrome, as a co-regulator of p63 responsive genes. Examination of p63 binding sites in neonatal foreskin keratinocytes

2012-06-07 | E-GEOD-32061 | biostudies-arrayexpress

p63 cooperates with CTCF to modulate chromatin accessibility and architecture in skin keratinocytes

Project description:Here we integrated multi-omics profiles including transcriptomics, DNA accessibility and capture Hi-C data to explore how p63 shapes local chromatin architecture in skin keratinocytes isolated from EEC syndrome patients. Surprisingly, we observed decreased chromatin accessibility in a number of DNA looping nodes which were co-mediated by p63 and CTCF. Our findings not only identified a new aspect of the bookmark function of p63, but also shed light on the disease mechanism underlined p63 dysfunction. Therefore, we propose p63 as a spatial genome organizer by modulating a subset of DNA loops with CTCF and therefore fine-tuning transcription programs required for skin keratinocytes.

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Genome wide identification of p63 binding sites in human neonatal foreskin keratinocytes

2012-06-08 | GSE32061 | GEO

Impact of iASPP knockout on p63 genome occupancy in mouse keratinocytes

Project description:iASPP (PPP1R13L) is an evolutionarily conserved regulator of p53 family members. In mice, iASPP deletion in keratin 14-expressing keratinocytes is sufficient to cause detrimental phenotypes with squamous epithelium abnormalities. In human skin, wild-type nuclear iASPP colocalizes with the key squamous differentiation regulatory factor, TP63, and iASPP mutations are associated with abnormalities in skin development. To clarify how iASPP modulates p63 genome occupancy, p63 ChIP-seq data from iASPP WT and iASPP KO primary mouse keratinocytes (MKC) were compared.

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Gene expression profiles of p63 knockout mouse

Project description:p63 is essential for the self-renewal of stem cells of all stratified epithelial tissues, including mammary and prostate glands as well as all squamous epithelia. In p63 null embryos, stratified epithelial tissues are lost or eroded several days after stratification due to the loss of regenerative cell populations. Here we show that p63 null embryos rapidly develop intestine-like metaplasia with gene expression profiles similar to Barrett’s metaplasia in a proximal stomach region. Also, we found that deletion of p63 cells in bladder leads to an expansion of columnar epithelial cells along the basement membrane and their rapid transition to a metaplastic phenotype similar to Barrett’s esophagus. It is likely that bladder carcinogens recapitulate this entire metaplastic transition.

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Chromatin modification is not a prerequisite for p63 binding but p63 binding can elicit chromatin remodeling

Project description:Transcription factor (TF) p63 is a master regulator playing critical roles in epidermal development and other cellular processes. Our lab’s previous research deciphered a distinct chromatin architecture at p63 bound site in keratinocytes. In order to figure out whether those chromatin modifications already exist before p63 binding, or p63 occupancy contributes to such chromatin marks, we built p63-expressing cell lines. We then obtained p63 bound regions in these overexpressing cell line, and looked at different histone marks at those sites before p63 occupancy. As shown in the results, before p63 binding, the targeting sites have barely detectable histone marks, indicating p63’s capability to approach unmodified chromatins. Moreover, there is no significant difference in chromatin marks between p63 bound sites and unbound sites when no p63 binding happens. Our in vivo findings were confirmed by examining p63 binding to unmodified nucleosomes in vitro, showing that histone modification is not indispensable for p63 binding but binding site positioning on nucleosome does play a role. Overall, our results suggest that histone modifications do not affect p63 binding, and p63 protein can bind to inaccessible, weakly modified chromatin regions in vivo.

2020-12-01 | GSE140329 | GEO

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