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Effect of YAP5SA expression on the transcriptome of proliferating and senescent cells

ABSTRACT: Effect of YAP5SA expression on the transcriptome of proliferating and senescent cells

PROVIDER: PRJNA1167311 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30842644_1.fastq.gz	Fastqsanger.gz
	SRR30842644_2.fastq.gz	Fastqsanger.gz
	SRR30842645_1.fastq.gz	Fastqsanger.gz
	SRR30842645_2.fastq.gz	Fastqsanger.gz
	SRR30842646_1.fastq.gz	Fastqsanger.gz

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Effect of YAP5SA expression on the transcriptome of proliferating and senescent cells

Project description:We have generated IMR90-hTERT cells carrying a Doxycyclin-inducible (Tet-On) vector expressing an N-terminally Flag tagged YAP5SA. To identify differentially expressed genes by YAP5SA expression during cellular senescence, we performed transcriptional profiling by RNA sequencing (RNA-seq) with or without YAP5SA expression (using doxycyclin), before and after senescence induction using a stress-induced senescence model (bleomycin-induced senescence).

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Expression data from proliferating and senescent murine hepatic stellate cells

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Genome-wide methylation maps for Proliferating and Senescent cells

Project description:Altered DNA methylation and associated destabilization of genome integrity and function is a hallmark of cancer. Replicative senescence imposes a limit on proliferative potential that all cancer cells must bypass. Compared to proliferating cells, senescent cells exhibit marked chromatin re-organization. Here we show by whole-genome single-nucleotide bisulfite sequencing that replicative senescent human cells exhibit widespread alterations in their DNA methylome. These changes are linked to mislocalization of the maintenance DNA methyltransferase (DNMT1) in cells approaching senescence, altered replication-coupled DNA methylation and de-repression of repetitive satellite sequences. Deficiency of DNMT1 triggers chromatin changes characteristic of senescence and expression of satellite sequences. Most importantly, but paradoxically, gains and losses of methylation in replicative senescence are similar to those in cancer, and this M-bM-^@M-^XreprogrammedM-bM-^@M-^Y methylation landscape is largely retained when cells escape or bypass senescence. In sum, altered regulation of DNMT1 in cells approaching replicative senescence contributes to changes in chromatin structure and function. Consequently, if senescent cells escape the proliferative barrier, they already harbor epigenetic changes likely to promote malignancy. Examination of methylation status in IMR90 cells

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