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TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [ATAC-seq]

ABSTRACT: TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [ATAC-seq]

PROVIDER: PRJNA939545 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23641129_1.fastq.gz	Fastqsanger.gz
	SRR23641129_2.fastq.gz	Fastqsanger.gz
	SRR23641130_1.fastq.gz	Fastqsanger.gz
	SRR23641130_2.fastq.gz	Fastqsanger.gz
	SRR23641131_1.fastq.gz	Fastqsanger.gz

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TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions

Project description:TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions

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TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [CUT&Tag]

Project description:TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [CUT&Tag]

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TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [RNA-seq]

Project description:TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [RNA-seq]

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TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [CUT&Tag]

Project description:Dramatic alterations in epigenetic landscapes are known to affect genome accessibility and their transcriptional program. Extensive evidences have emerged that senescent cells accumulate profound chromatin tremendous reordering upon senescence entry, yet, the underlying mechanisms between epigenetic parameters and gene expression profile have not been fully clarified. In this report, we delineate the genome-wide redistribution of accessible chromatin regions leading to broad transcriptome effects during UC-MSCs senescence. We report the distinct senescence-activated accessibility regions (SAAs) are always distributed in H3K27ac decorated enhancer regions, where the SAAs are responsible for elevated flanking SASP expression and aberrant cellular signaling relevant to SASP secretion. Mechanistically, a single transcription factor, TEAD4, shifting away from H3K27ac-labled SAAs and leading to prominent chromatin accessibility reconstruction during senescence. The enhanced signal of SAAs driven by TEAD4 suppression subsequently induce a robust decrease of adjacent SASP genes expression and downstream factors secretion, and finally, contributing to the progression of senescence. Our findings illustrate a dynamic landscape of chromatin accessibility following senescence entry and reveal an insightful function for TEAD4 in regulating the broad chromatin state that modulate the overall transcriptional program of the SASP genes.

2023-04-01 | GSE226294 | GEO

TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [ATAC-seq]

2023-04-01 | GSE226287 | GEO

TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions [RNA-seq]

2023-04-01 | GSE226325 | GEO

TEAD4 delays cellular senescence by remodeling chromatin accessibility at H3K27ac-occupied enhancer regions

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

2023-04-01 | GSE226326 | GEO

TEAD4 occupied genes in differentiated C2C12 myoblasts

Project description:The TEAD (1-4) transcription factors comprise the conserved TEA/ATTS DNA binding domain recognising the MCAT element in the promoters of muscle-specific genes. Despite extensive genetic analysis, the function of TEAD factors in muscle differentiation has proved elusive due to redundancy amongst the family members. Expression of the TEA/ATTS DNA binding domain that acts a dominant negative repressor of TEAD factors in C2C12 myoblasts inhibits their differentiation, while selective shRNA knockdown of TEAD4 results in abnormal differentiation characterised by the formation of shortened myotubes. Chromatin immunoprecipitation coupled to array hybridisation (ChIP-chip) shows that TEAD4 occupies 867 promoters including those of myogenic miRNAs. We show that TEAD factors cooperate with MYOD1 to directly induce Myogenin, CDKN1A and Caveolin 3 expression to promote myoblast differentiation and fusion. RNA-seq identifies a novel set of TEAD4 target genes encoding muscle structural and regulatory proteins and those required for the unfolded protein response. In contrast, TEAD4 represses expression of the growth factor CTGF and Cyclin D1 to promote differentiation. Together these results show that TEAD factor activity is essential for C2C12 cell differentiation and define a novel and nonredundant role for TEAD4 in regulating the unfolded protein response. C2C12 cells were infected with retrotiviral vector expressing Flag-HA-Tagged TEAD4 or with empty control vector and selected in the continouos presence of puromycin. Infected cell populations were then differentiated for 5 days in DMEM medium with 2% horse serum and fixed in 0.4% formaldehyde.

2011-08-21 | E-GEOD-29208 | biostudies-arrayexpress

TEAD4 occupied genes in differentiated C2C12 myoblasts

2011-08-22 | GSE29208 | GEO

TEAD4

Project description:TEAD4

| PRJNA604980 | ENA