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Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, with or without TSA treatment.

ABSTRACT: Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, with or without TSA treatment.

PROVIDER: PRJNA547766 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9214730_1.fastq.gz	Fastqsanger.gz
	SRR9214730_2.fastq.gz	Fastqsanger.gz
	SRR9214731_1.fastq.gz	Fastqsanger.gz
	SRR9214731_2.fastq.gz	Fastqsanger.gz
	SRR9214722_1.fastq.gz	Fastqsanger.gz

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Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, with or without TSA treatment.

Project description:Gene expression changes were compared in proliferating and senescent human IMR90 cells, with or without TSA treatment. Method: RNA was extracted, in triplicate, then sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Tophat2 and then analysed with Cufflinks.

2020-06-30 | GSE132370 | GEO

Expression data from proliferating and senescent IMR90 cells

Project description:Total RNA was isolated from proliferating and senescent IMR90 cells to compare gene-expression to the changes in nucleolus-association in proliferating and senescent IMR90 cells.

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Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, expressing either empty vector or Parkin, with or without CCCP treatment

Project description:Gene expression changes were compared in proliferating and senescent human IMR90 cells, with either empty vector, Parkin, or Parkin+CCCP. Method: RNA was extracted, in triplicate, then sequenced with an Illumina NextSeq 500 sequencer. Sequence reads passing the quality control filters were aligned using Tophat2 and then analysed with Cufflinks.

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Phosphorylation level of SIRT1 in proliferating and senescent IMR90 cells

Project description:Mammalian SIRT1 is a central regulator of metabolism and aging. This project is to analyze global phosphorylation levels of mammalian SIRT1 in proliferating and senescence states using human lung fibroblast IMR90, in order to explore the post-translational regulation of SIRT1 protein upon cellular senescence and its potential roles in the regulatory mechanisms of SIRT1 homeostasis.

2020-09-29 | PXD020081 | Pride

Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, expressing either empty vector or Parkin, with or without CCCP treatment

Project description:Deep sequencing of human fibroblastic cell line IMR90, either proliferating or senescent, expressing either empty vector or Parkin, with or without CCCP treatment

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Genome-wide mapping of H4K20me3 in proliferating and senescent IMR90 cells.

Project description:Cellular senescence is a stable proliferation arrest and tumor suppressor mechanism. Abundance of histone modification, H4K20me3, has been reported to increase in senescent cells. Generally, H4K20me3 promotes formation of compacted transcriptionally silent constitutive heterochromatin, but its specific role in senescence is unknown. Here, we show that in senescent cells H4K20me3 is enriched at specific families of gene repeats (ZNFs, Olfactory Receptors, Protocadherins), and DNA sequences contained within senescence-associated heterochromatin (senescence-associated heterochromatin (SAHF)). Furthermore, in senescent cells, but not proliferating cells, H4K20me3 is also markedly enriched at bodies of repressed genes, including proliferation-promoting genes. Ectopic expression of SUV420H2, responsible for deposition of H4K20me3, reinforces senescence-associated proliferation arrest, and slows proliferation of transformed cells and tumorigenesis in vivo. These results indicate a dedicated role for H4K20me3 in control of nuclear organization and gene expression in senescent cells and stable senescence-associated proliferation arrest and tumor suppression.

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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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