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RNAseq of Normal Human Epidermal Keratinocytes (NHEKs) in UVB-induced senescence (UVB-SIPS, at 3 days or 5 days) or in replicative-like senescence (RS)

ABSTRACT: RNAseq of Normal Human Epidermal Keratinocytes (NHEKs) in UVB-induced senescence (UVB-SIPS, at 3 days or 5 days) or in replicative-like senescence (RS)

PROVIDER: PRJEB47682 | ENA |

REPOSITORIES: ENA

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RNAseq of Normal Human Epidermal Keratinocytes (NHEKs) in UVB-induced senescence (UVB-SIPS, at 3 days or 5 days) or in replicative-like senescence (RS)

Project description:RNAseq analyses of NHEKs in replicative-like senescence, i.e. in growth arrest after about ten passages in culture, or in premature senescence induced by repeated UVB exposures (UVB-SIPS), at 3 days and at 5 days after the last UVB stress.

2022-12-31 | E-MTAB-10969 | biostudies-arrayexpress

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Unveiling E2F4, TEAD1 and AP-1 as regulatory transcription factors of the replicative senescence program by multiomics analysis

Project description:Senescence, a stable state of growth arrest, affects many physiological and pathophysiological processes, especially aging. Previous work has indicated that transcription factors (TFs) play a role in regulating senescence. However, a systematic study of regulatory TFs during replicative senescence (RS) using multi-omics analysis is still lacking. Here, we generated time-resolved RNA-seq, reduced representation bisulfite sequencing (RRBS) and ATAC-seq datasets during RS of mouse skin fibroblasts, which demonstrated that an enhanced inflammatory response and reduced proliferative capacity were the main characteristics of RS in both the transcriptome and epigenome. Through integrative analysis and genetic manipulation, we found that transcription factors E2F4, TEAD1 and AP-1 are key regulators of RS. Overexpression of E2f4 improved cellular proliferative capacity, attenuated SA-β-Gal activity and changed RS-associated differentially methylated sites (DMSs). Moreover, knockdown of Tead1 attenuated SA-β-Gal activity and partially altered the RS-associated transcriptome. In addition, knockdown of Atf3, one member of AP-1 superfamily TFs, reduced Cdkn2a (P16) expression in pre-senescent fibroblasts. Taken together, results of this study identified transcription factors regulating the senescence program through multi-omics analysis, providing potential therapeutic targets for anti-aging.

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Project description:We stably infected IMR90 fibroblasts with lentiviral vectors expressing doxycycline-inducible TRF2dBdM or vector control. Cells were treated with 1mg/ml of doxycycline for 7 days to induce senescence in the cells expressing TRF2dBdM before collecting RNA. IMR90 cells, either young (passage 10, population doubling ~20) or old (passage 24, population doubling ~40-48) were also used as a model of replicative senescence. The transcriptomes were analyzed using RNA microarrays.

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Project description:RS Rawdata

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Nuclear barrier induction as a new modality of cellular senescence

Project description:Blocking of nucleocytoplasmic trafficking is an essential feature of replicative senescence (RS). However, whether nuclear barrier per se causes cellular senescence still remains elusive. Here, we show that nuclear barrier induced by blocking nucleocytoplasmic trafficking, especially nuclear export, elicits RS-like changes in SA-β-gal activity, DNA damage, and expression of cell cycle regulators. Comparative transcriptome analysis revealed that nuclear barrier-induced senescence (NBIS) was most similar in gene expression changes to RS compared to senescence induced by stresses (oxidative stress, DNA damage and oncogene), implying that nuclear barrier induces RS-like physiological senescence-associated changes. Shared senescence-related processes between NBIS and RS included lysosomal degradation, nuclear transport, and translation, resulting in coordinated reduction in transmission of extrinsic signals to nucleus and intracellular protein supply from nucleus. Notably, these processes were conserved in yeast aging. Therefore, we propose NBIS as a novel modality of cellular senescence, representing the fundamental nature of physiological aging in eukaryotes.

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Cellulosimicrobium sp. RS strain:RS

Project description:Cellulosimicrobium sp. RS strain:RS Genome sequencing

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ralstonia solanacearum Rs strain:Rs

Project description:ralstonia solanacearum Rs strain:Rs Genome sequencing

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Disruption of nucleocytoplasmic trafficking as a cellular senescence driver

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