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Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler

ABSTRACT: Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler

PROVIDER: PRJNA860788 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20339910_1.fastq.gz	Fastqsanger.gz
	SRR20339910_2.fastq.gz	Fastqsanger.gz
	SRR20339912_1.fastq.gz	Fastqsanger.gz
	SRR20339912_2.fastq.gz	Fastqsanger.gz
	SRR20339913_1.fastq.gz	Fastqsanger.gz

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Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq]

Project description:Alu retrotransposons, forming the largest family of mobile DNA elements in the human genome, have recently come to attention as a potential source of regulatory novelties, most notably by participating in enhancer function. Even though Alu transcription by RNA polymerase III is subjected to tight epigenetic silencing, their bulk expression has long been known to increase in response to various types of stress, including viral infection. Here we show that, in primary human fibroblasts, adenovirus small e1a triggered derepression of hundreds of individual Alus, by promoting TFIIIB recruitment by Alu-bound TFIIIC. Epigenome profiling revealed an e1a-induced decrease of H3K27 acetylation and increase of H3K4 monomethylation at derepressed Alus, making them resemble poised enhancers. The enhancer nature of e1a-targeted Alus was confirmed by the enrichment, in their upstream regions, of the EP300/CBP acetyltransferase and of the YAP1 and FOS transcription factors. The physical interaction of e1a with the chromatin remodeler EP400 turned out to be critical for Alu derepression, and upstream enrichment of EP400 was found to commonly demarcate expression-prone Alus. Our data suggest that e1a targets a subset of enhancer Alus whose transcriptional activation, mediated by e1a-EP400 interaction, may participate in the manipulation of enhancer activity by adenovirus.

2024-03-31 | GSE208716 | GEO

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

2024-03-31 | GSE208685 | GEO

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq]

Project description:Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [RNA-Seq]

| PRJNA860793 | ENA

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

Project description:Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler [ChIP-Seq]

| PRJNA860610 | ENA

Adenovirus small E1A directs activation of Alu transcription at YAP/TEAD- and AP-1- bound enhancers through interactions with the EP400 chromatin remodeler

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

2024-03-31 | GSE208717 | GEO

Expression changes in mouse oligodendrocytes after deletion of the Ep400 chromatin remodeler

Project description:To address the role of INO80/SWR-type remodeling complexes, we deleted Ep400 at defined times of mouse oligodendrocyte development. Whereas oligodendrocyte precursors are specified and develop normally without Ep400, terminal differentiation is dramatically impaired resulting in hypomyelination. RNA-Seq studies were performed on cultured and FACS sorted control and Ep400-deficient mouse oligodendrocytes to analyze changes in gene expression. These revealed that genes associated with the myelination program and with response to DNA damage are altered in Ep400-deficient oligodendrocytes.

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De-differentiation by Adenovirus E1A Due to Inactivation of Hippo Pathway Effectors YAP and TAZ [RNA-seq]

Project description:Adenovirus-transformed cells have a de-differentiated phenotype. Eliminating E1A in transformed human embryonic kidney cells de-repressed ~2600 genes, generating a gene expression profile closely resembling mesenchymal stem cells (MSC). This was associated with a dramatic change in cell morphology from one with scant cytoplasm and a globular nucleus to one with increased cytoplasm, extensive actin stress fibers and actomyosin-dependent flattening against the substratum. E1A-induced histone hypoacetylation by p300/CBP at H3K27/18 was reversed. Most of the increase in H3K27/18ac was near TEAD transcription factors associated with their co-activators YAP and TAZ regulated by the Hippo pathway. E1A causes YAP/TAZ cytoplasmic sequestration. After eliminating E1A, YAP/TAZ were transported into nuclei where they associated with poised enhancers with DNA-bound TEAD4 and H3K4me1. This activation of YAP/TAZ required RHO-family GTPase signaling and caused histone acetylation by p300/CBP, chromatin remodeling, and cohesin loading to establish MSC-associated enhancers and then super-enhancers. Consistent results were also observed in rat embryo kidney cells, human fibroblasts and human respiratory tract epithelial cells. These results together with earlier studies suggest that YAP/TAZ function in a developmental check-point controlled by signaling from the actin cytoskeleton that prevents differentiation of a progenitor cell until it is in the correct cellular and tissue environment.

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De-differentiation by Adenovirus E1A Due to Inactivation of Hippo Pathway Effectors YAP and TAZ [ChIP-seq]

2019-06-01 | GSE130135 | GEO

De-differentiation by Adenovirus E1A Due to Inactivation of Hippo Pathway Effectors YAP and TAZ [ATAC-seq]

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Adenovirus E1A oncogene induces re-replication of cellular DNA and alters DNA replication dynamics

Project description:Human adenovirus type 5 oncogene E1A was shown to induce massive re-replication of cellular DNA in late S phase. Using DNA combing analysis, it was shown that DNA replication dynamics including replicon length, fork velocity and inter-origin distance were dramatically altered in E1A expressing cells as compared to that of normal serum stimulated cells. It was also shown that c-Myc that is induced in E1A expressing cells is essential for the efficient entry of E1A expressing cells into S phase.

2013-05-22 | GSE47140 | GEO

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