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CPSF controls PAS selection and epidermal differentiation

ABSTRACT: CPSF controls PAS selection and epidermal differentiation

PROVIDER: PRJNA524364 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10109434.fastq.gz	Fastqsanger.gz
	SRR10109435.fastq.gz	Fastqsanger.gz
	SRR10109436.fastq.gz	Fastqsanger.gz
	SRR10109437.fastq.gz	Fastqsanger.gz
	SRR10109438.fastq.gz	Fastqsanger.gz

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CPSF controls PAS selection and epidermal differentiation

Project description:Alternative polyadenylation (APA) is a regulatory mechanism that controls gene expression level and function through the usage of different transcription termination sites, but how APA is regulated to influence epidermal tissue differentiation remains under-characterized. Leveraging 3’READS+, we identified prevalent APA in keratinocytes. We further identified a high-confidence list of genes that alters their usages of polyadenylation site (PAS) during keratinocyte differentiation. To begin to understand the mechanisms that modulates PAS selection within a given gene, we identified that the expression of the Cleavage and Polyadenylation Specificity Factor (CPSF) complex is down regulated during keratinocyte differentiation. Suppression of CPSF using RNAi or CRISPRi strongly impaired epidermal regeneration with upregulation of terminal differentiation marker gene expression. Mechanistically, we identified that CPSF suppression decreased the usage of the GRHL3 proximal PAS and upregulated full-length GRHL3 mRNA production. Knockdown of GRHL3 in the context of CPSFi partially restored differentiation marker gene expression. We also found CPSF interacts with RNA-binding proteins to control PAS usage. Thus, our data suggest a model where CPSF binding preference and PAS choices regulate epidermal terminal differentiation.

2020-11-02 | GSE127223 | GEO

The dynamic, combinatorial cis-regulatory lexicon of epidermal differentiation [PAS-seq]

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The dynamic, combinatorial cis-regulatory lexicon of epidermal differentiation [PAS-seq]

Project description:A deep-learning framework interprets multi-omic data across epidermal differentiation, identifying cooperative DNA sequence rules that regulate gene modules. Massively parallel reporter analysis validates temporal dynamics and cis-regulatory logic.

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The phosphatase regulator NIPP1 controls epidermal homeostasis

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The M3 Muscarinic Acetylcholine Receptor Promotes Epidermal Differentiation

Project description:The M3 muscarinic acetylcholine receptor (CHRM3) is predominantly expressed in the basal epidermal layer where it mediates the effects of the auto/paracrine cytotransmitter acetylcholine. Patients with the autoimmune blistering disease pemphigus develop autoantibodies to CHRM3 and show alterations in keratinocyte adhesion, proliferation and differentiation, suggesting that CHRM3 controls these cellular functions. Chrm3 mice display altered epidermal morphology resembling that seen in patients with pemphigus vulgaris. Here, we characterized the cellular and molecular mechanisms whereby CHRM3 controls epidermal structure and function. We used single cell (sc)RNA-seq to evaluate keratinocyte heterogeneity and identify differentially expressed genes in specific subpopulations of epidermal cells in Chrm3 KO neonatal mice.

2022-05-06 | GSE201885 | GEO

Comparison of MBT/Pas and BALB/cByJ MEFs response after infection with Rift Valley Fever virus

Project description:The Rift Valley Fever (RVF) is an arthropod-borne disease present in several countries of Africa and Middle East. It is caused by RVF virus which can infect both humans and animals. In humans, it leads to various manifestations including hepatitis, encephalitis and death, while in domestic animals it usually causes miscarriage in pregnant females and it is often fatal for the newborn. Not all people or animal infected by the virus present the same disease. Some patients exhibit unapparent or moderate febrile reactions, while others develop severe symptoms. This observation suggests that host genetic factors play a role in controlling the outcome of infection. In this work, we compare the response of two different inbred strains of mice, MBT/Pas and BALB/cByJ, to infection with RVF virus. These strains exhibit different profiles of susceptibility to RVF virus infection. Indeed, MBT/Pas mice rapidly develop high viraemia and die soon after infection, while BALB/cByJ mice have a lower viraemia and die later. Interestingly, mouse embryonic fibroblasts (MEFs) obtained from MBT/Pas foetuses allows higher viral production than BALB/cByJ MEFs. Keywords: expression profiling The experiment was designed to include ARN samples from MBT/Pas and BALB/cByJ MEFs infected with the Rift Valley Fever (RVF) virus, and their respective mock-infected controls; each one of those in triplicate. Therefore, we have used 12 different samples for the study, divided as follows: 3 samples of RVF virus-infected BALB/cByJ MEFs, 3 samples of mock-infected BALB/cByJ MEFs, 3 samples of RVF virus-infected MBT/Pas MEFs and 3 samples of mock-infected MBT/Pas MEFs. Each RNA was extracted from a different culture well.

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ΔNp63-Senataxin circuit controls keratinocyte differentiation by promoting the transcriptional termination of epidermal genes

Project description:ΔNp63-Senataxin circuit controls keratinocyte differentiation by promoting the transcriptional termination of epidermal genes

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ΔNp63-Senataxin circuit controls keratinocyte differentiation by promoting the transcriptional termination of epidermal genes

Project description:ΔNp63, a master regulator of epithelial biology, is involved in regulating epithelial stem cell function, maintaining the integrity of stratified epithelial cells and committing epidermal cells to the differentiation program. To this end, ΔNp63 exploits several direct mechanisms. Here, we elucidated a novel mechanism whereby ΔNp63 efficiently sustains the expression of epidermal differentiation genes. We show that ΔNp63 interacts with Senataxin (SETX), an RNA/DNA helicase able to resolve the R-loop intermediates over the GC-rich termination sites of coding genes. Notably, we found that SETX and ΔNp63 co-regulate a subset of genes involved in the early step of the keratinocyte differentiation program. At the molecular level, SETX physically binds the p63 DNA binding motifs present in two early epidermal differentiation genes, Keratin 1 (KRT1) and ZNF750, facilitating R-loop removal over their 3’ ends and thus promoting efficient transcriptional termination and gene expression. Remarkably, SETX loss affects the activation of the proper epidermal differentiation program in vitro and impacts epidermal layer stratification in organotypic human skin. Furthermore, we found that SETX is mutated or downmodulated in SCC and SETX gene mutation is a negative prognostic factor for cutaneous SCC patient survival. Collectively, our results unveil SETX as a novel molecular player of skin homeostasis, potentially involved in hyperproliferative skin disorders.

2022-01-10 | GSE193205 | GEO

The long non-coding RNA LINC00941 modulates MTA2/NuRD occupancy to suppress premature human epidermal differentiation

Project description:Numerous long non-coding RNAs (lncRNAs) were shown to have functional impact on cellular processes, such as human epidermal homeostasis, but for only a few the mode of action has been elucidated. Here, we report that lncRNA LINC00941 controls keratinocyte differentiation on a global level through association with the MTA2/NuRD complex, one of the major chromatin remodelers in cells. LINC00941 was found to interact with NuRD-associated MTA2, suppressing the expression of the transcription factor EGR3, a regulator of epidermal differentiation. Both LINC00941 and the MTA2/NuRD complex are enriched in non-differentiated keratinocytes and repress the expression of differentiation genes through epigenetic silencing of EGR3, consequentially preventing premature differentiation of human progenitor cells.

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2012-02-02 | E-GEOD-35468 | biostudies-arrayexpress

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