Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA126927 | ENA |
REPOSITORIES: ENA
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Project description:Pre-mRNA splicing is functionally coupled to transcription, and genotoxic stresses can enhance alternative exon inclusion by affecting elongating RNA polymerase II. We report here that various genotoxic stress inducers, including camptothecin, inhibit the interaction between EWS, an RNA polymerase II-associated factor, and YB-1, a spliceosome-associated factor. This results in the cotranscriptional skipping of several exons of the MDM2 gene encoding the main p53 ubiquitin-ligase. This reversible exon skipping participates in the timely regulation of MDM2 expression, and may contribute to the accumulation of p53 during stress exposure and its rapid shut off when stress is removed. Finally, a splicing-sensitive microarray identified numerous exons that are skipped in response to camptothecin and EWS/YB-1 depletion. These data demonstrate genotoxic stress-induced alteration of the communication between the transcriptional and splicing machineries, resulting in widespread exon skipping and playing a central role in the genotoxic stress response. 6 samples of MCF7 cells exposed to different treatments were analyzed: 3 x control_6 hours; 3 x camptothecin_6 hours.
2010-06-09 | E-GEOD-21840 | biostudies-arrayexpress
Project description:Pre-mRNA splicing is functionally coupled to transcription, and genotoxic stresses can enhance alternative exon inclusion by affecting elongating RNA polymerase II. We report here that various genotoxic stress inducers, including camptothecin, inhibit the interaction between EWS, an RNA polymerase II-associated factor, and YB-1, a spliceosome-associated factor. This results in the cotranscriptional skipping of several exons of the MDM2 gene encoding the main p53 ubiquitin-ligase. This reversible exon skipping participates in the timely regulation of MDM2 expression, and may contribute to the accumulation of p53 during stress exposure and its rapid shut off when stress is removed. Finally, a splicing-sensitive microarray identified numerous exons that are skipped in response to camptothecin and EWS/YB-1 depletion. These data demonstrate genotoxic stress-induced alteration of the communication between the transcriptional and splicing machineries, resulting in widespread exon skipping and playing a central role in the genotoxic stress response.
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Project description:Psychological stress reactions can stimulate mammalian immune functions due to yet unknown mechanisms. We hypothesized that these involve massive post-stress alternative splicing modulations in peripheral blood mononuclear cells (PBMCs). RNA was extracted from PBMCs of BALB/C mice following unpredictable repeated foot shocks. Among the tested group, five mice exhibiting the maximal circulation glucocorticoids were selected for the stress group. PBMC RNA of 5 BALB/C mice served as the control group. Through linear regression analysis of all the reciprocal junction pairs represented on the microarrays and the Ensembl database, 496 alternative splicing events were detected. The stressed mice showed 65% exon skipping out of total splicing event changes compared to controls. The detected genes exhibited functional enrichment (through DAVID EASE analysis) in alternative splicing (47%), cellular response to stress (12%), lymphocyte activation (8%), stress-induced proteins (2%) and heat-shock-induced proteins (2%). Specifically, exon skipping modifications in the Hnrnph1 and CLK1 splicing-related transcripts were accompanied by stress-inducible inclusions in the immune response-related IRF-1 gene. Our findings demonstrate dependence on exon skipping and independence from glucocorticoid and innate immunity for the stress-inducible exacerbation of immunity and open new venues for preventing post-trauma inflammatory crisis.
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