Analysis of senescence transcriptome upon knockdown of XPO7 [RNA-seq]
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE153921 | GEO | 2021/02/12
REPOSITORIES: GEO
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Project description:We used IMR90 ER:RAS cells infected with an empty vector or an shRNA for ARID1B and induced senescence by addition of 4OHT. 6 days later RNA was collected for gene expression analysis. With a functional screen we previously identified ARID1B as a new regulator of cellular senescence. By performing gene expression analysis we confirmed this finding and showed that knockdown of ARID1B prevents the expression of genes induced during senescence.
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Project description:The goal of this study was to compare the transcriptomics of different forms of senescence with each other and to normal growing and quiescent IMR90 cells.Senescence was induced in IMR90 cells by different stimuli. Therapy-induced senescence was induced by treatment with doxorubicin, irradiation, etoposide and palbociclib. Oncogene-induced senescence was induced by addition of tamoxifen (4OHT) to IMR90 ER:RAS cells.
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Project description:Senescence can be transmitted in a paracrine way from cells undergoing Oncogene Induced Senescence (OIS) to naM-CM-/ve normal cells. We define this phenomenon as M-bM-^@M-^\paracrine senescenceM-bM-^@M-^] We used microarrays to compare the trancriptome of cells undergoing paracrine senescence to the transcriptome of cells suffering OIS to unveil the common signatures defining both events and the similarities between them IMR90 cells were co-cultured with IMR90 ER:RAS undergoing OIS or IMR90-Vector control cells using 0.2 M-NM-<m pore transwell (anopore) to allow communication of soluble factors but physical separation of the two cell populations. The total mRNA of IMR90, IMR90 ER:RAS or IMR90 cells cultured in Transwells together with IMR90 vector or IMR90 ER:RAS cells during 7 days in the presence of 200 nM 4OHT and 0.5 % FBS was extracted and hybridized on Affymetrix microarrays to compare paracrine senescence to OIS.
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Project description:IMR90 ER:RAS cells were infected with 2 different lentiviral pGIPZ shRNAs against AHCY or with an empty vector (EV). We treated IMR90 ER:RAS cells with 4OHT to induce RAS activation or with vehicle (DMSO) as a non-senescent control. RNA was collected 6 days after the start of the experiment once the senescence program has been fully implemented. Our previous experiments showed that knockdown of AHCY prevents senescence. By performing RNAseq, we have unveiled that AHCY knockdown prevents upregulation of a set of genes essential for the onset of senescence and its associated secretory phenotype.
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Project description:We expressed either a wt or a phosphomutant version of ZFP36L1 in IMR90 ER:RAS cells. 7 days upon RAS induction (when the cells reach a fully senescent phenotype) we collected the RNA. ZFP36L1 is a RNA binding protein that binds to AU-rich elements in the 3âUTR of mRNAs and triggers their degradation. Our previous experiments showed that the activity of ZFP36L1 was key in the regulation of the senescent phenotype.By performing RNAseq we have uncovered the effect of expressing a constitutively active mutant of ZFP36L1 within the senescent transcriptome. 4 samples examined: Non-senescent cells (EV - 4OHT), Senescent cells (EV + 4OHT), Senescent cells expressing ZFP36L1wt and Senescent cells expressing ZFP36L1mut
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Project description:The expansion of repressive epigenetic marks has been implicated in heterochromatin formation during embryonic development, but the general applicability of this mechanism is unclear. Here we show that nuclear rearrangement of repressive histone marks H3K9me3 and H3K27me3 into non-overlapping structural layers characterizes senescence-associated heterochromatic foci (SAHF) formation in human fibroblasts. However, the global landscape of these repressive marks remains unchanged upon SAHF formation, suggesting that in somatic cells heterochromatin can be formed through the spatial repositioning of pre-existing repressively marked histones. This model is reinforced by the correlation of pre-senescent replication timing with both the subsequent layered structure of SAHFs and the global landscape of the repressive marks, allowing us to integrate microscopic and genomic information. Furthermore, modulation of SAHF structure does not affect the occupancy of these repressive marks nor vice versa. These experiments reveal that high-order heterochromatin formation and epigenetic remodeling of the genome can be discrete events. ChIP-seq for different histone marks in both growing and Ras-induced senescent fibroblasts, in the presence or absence of certain sh-RNAs K9me3Grow2.bed (growing) Chip Seq Analysis of H3K9me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K9me3Sen2.bed (senescent) Chip Seq Analysis of H3K9me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K9me2Grow3.bed (growing) Chip Seq Analysis of H3K9me2 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K9me2Sen3.bed (senescent) Chip Seq Analysis of H3K9me2 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K27me3Sen3.bed (senescent) Chip Seq Analysis of H3K27me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K27me3Grow2.bed (growing) Chip Seq Analysis of H3K27me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K36me3Grow2.bed (growing) Chip Seq Analysis of H3K36me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K36me3Sen2.bed (senescent) Chip Seq Analysis of H3K36me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT K4me3Grow2.bed (growing) Chip Seq Analysis of H3K4me3 in ER:Ras expressing IMR90 human diploid fibroblasts with no treatment K4me3Sen3.bed (senescent) Chip Seq Analysis of H3K4me3 in ER:Ras expressing IMR90 human diploid fibroblasts d6 4OHT
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Project description:To determine the transcriptional function (if any) of the presumed nuclear export protein Xpo7 or RanBP16 Murine fetal liver erythroid precursors (Ter119-negative cells) were isolated from C57Bl6 E14.5 embryos by magnetic depletion and infected with retroviruses containing shRNA constructs against Xpo7. They were then cultured in Epo-containing media (2U/mL) for 36hrs until they were fully differentiated and then sorted by FACS for GFP+ (infected) cells in order to isolate total RNA to be used for the profiling.
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Project description:We treated IMR90 ER:RAS cells with 4OHT to induce RAS activation or with vehicle (DMSO) as a non-senescent control. At the same time, cells were treated with 10 µM 3-deaazadenosine. 3-deazaadenosine is a SAM-dependent methyltransferase inhibitor. H3K36me3 is a mark enriched at actively transcribed genes. Our previous experiments showed that treatment with 3-deazaadenosine prevents senescence and reduces overall levels of H3K36me3. By performing ChIP-seq, we have unveiled that treatment with 3-deazaadenosine prevents deposition of H3K36me3 in genes essential for the secretory phenotype of senescent cells.
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