P38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress
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ABSTRACT:
PROVIDER: PRJNA482978 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7602010_1.fastq.gz | Fastqsanger.gz | |||
| SRR7602010_2.fastq.gz | Fastqsanger.gz | |||
| SRR7602011_1.fastq.gz | Fastqsanger.gz | |||
| SRR7602011_2.fastq.gz | Fastqsanger.gz | |||
| SRR7602012_1.fastq.gz | Fastqsanger.gz |
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Project description:Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK. Remarkably, a splicing network analysis revealed a functional connection between p38 and the spliceosome component SKIIP. Depletion of SKIIP abolished a significant part of the p38-mediated alternative splicing.
2019-04-16 | GSE117699 | GEO
Project description:Cells have the ability to respond and adapt to environmental changes through the activation of stress-activated protein kinases (SAPKs). Although it has been shown that p38 SAPK signalling participates in the regulation of gene transcription, there is not a comprehensive genome-wide transcription study reported to date describing neither the role of the p38 SAPK on the immediate response to stress and its kinetics nor a comparative vision of the genes that respond to different stimuli that activate the p38 SAPK. Here, we report a whole genome microarray analyses on wild type mouse embryonic fibroblasts (MEFs) treated with different p38 SAPK activators, namely the physiological cytokine TNF alpha, the protein synthesis inhibitor antibiotic anisomycin and osmostress. In addition, we have analysed the contribution of p38 alpha the major isoform of p38 present in MEF cells, in the overall transcription in response to those stimuli by both, the inhibition of p38 SAPK by using a chemical inhibitor (SB203580) and the use of p38 alpha knock out MEFs. Furthermore, we have analysed the kinetics of the gene expression response to osmostress by the p38 SAPK. Two samples have been analysed; wild type Mouse embryonic fibroblast (WT-MEFs) and MAPK p38alfa knock out MEFs (KO-MEFs) respectively treated with 11 and 4 different treatments. Each experiment was performed in duplicate and referenced to a pool of two non-treated WT MEFs.
2010-09-29 | E-GEOD-18320 | biostudies-arrayexpress
Project description:Cells have the ability to respond and adapt to environmental changes through the activation of stress-activated protein kinases (SAPKs). Although it has been shown that p38 SAPK signalling participates in the regulation of gene transcription, there is not a comprehensive genome-wide transcription study reported to date describing neither the role of the p38 SAPK on the immediate response to stress and its kinetics nor a comparative vision of the genes that respond to different stimuli that activate the p38 SAPK. Here, we report a whole genome microarray analyses on wild type mouse embryonic fibroblasts (MEFs) treated with different p38 SAPK activators, namely the physiological cytokine TNF alpha, the protein synthesis inhibitor antibiotic anisomycin and osmostress. In addition, we have analysed the contribution of p38 alpha the major isoform of p38 present in MEF cells, in the overall transcription in response to those stimuli by both, the inhibition of p38 SAPK by using a chemical inhibitor (SB203580) and the use of p38 alpha knock out MEFs. Furthermore, we have analysed the kinetics of the gene expression response to osmostress by the p38 SAPK.
2010-09-29 | GSE18320 | GEO
Project description:HeLa cells were treated with 100 mM NaCl during 2h versus untreated. HeLa cells treated with 100 mM NaCl during 2h versus HeLa cells treated with 100 mM NaCl during 2h after pre-treatment with 10 μM SB203580 for 30 min. Alternative splicing is a crucial mechanism for gene regulation that is modulated in response to a wide range of extracellular stimuli. Stress-activated protein kinases (SAPKs) play a key role in controlling several steps of mRNA biogenesis. Here, we show that osmostress has a major impact on the regulation of alternative splicing (AS), which is partly mediated through the action of the p38 SAPK.
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Project description:Effect of p38 SAPK activation on HeLa cells
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Project description:The mitogen-activated protein kinase (MAPK) p38 signaling pathway is essential for normal heart function. However, p38 also contributes to heart failure pathogenesis by affecting heart contractility and cardiomyocyte survival. To unravel the complex cardiac role of p38, we report the interactome of p38α and p38γ, the two well expressed isoforms in the heart, obtained via an APEX proximity assay performed in cultured neonatal rat ventricular myocytes. The p38α and p38γ have distinct interactomes in cardiomyocytes for both studied states; basal and activated by an osmotic stress. Interestingly, the activated p38α interactome contains many spliceosome implicated RNA-binding proteins. The serine/arginine-rich splicing factor 3 (SRSF3) is of particular interest and its interaction with p38α was validated by co-immunoprecipitation. p38 is sufficient to partially relocate nuclear SRSF3 to cytoplasm. The alternative splicing function of SRSF3 is also modulated by the p38 pathway. Our findings reveal a novel set of proteins to investigate in order to decipher cardiac functions of the MAPK p38, as well as a specific regulation mechanism of SRSF3 by p38 in cardiomyocytes.
2021-03-01 | PXD011089 | Pride
Project description:Adaptation to altered osmotic conditions is a fundamental property of living cells and has been studied in particular detail in the yeast Saccharomyces cerevisiae. Yeast cells accumulate glycerol as compatible solute, controlled at different levels by the High Osmolarity Glycerol (HOG) response pathway. Up to now, essentially all osmostress studies in yeast have been performed with glucose as carbon and energy source, which is metabolised by glycolysis with glycerol is as a normal by-product. Here we investigated the response of yeast to osmotic stress when yeast is respiring ethanol as carbon and energy source. Remarkably, yeast cells do not accumulate glycerol under these conditions and it appears that trehalose may partly take over the role as compatible solute. The HOG pathway is activated in very much the same way as in during growth on glucose medium and is also required for osmotic adaptation. Slower volume recovery was observed in ethanol-grown cells as compared to glucose-grown cells. Dependence on key regulators as well as the global gene expression profile were similar in many ways to those previously observed in glucose-grown cells. However, there are indications that cells re-arrange redox-metabolism when respiration is hampered under osmostress, a feature that could not be observed in glucose-grown cells.
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Project description:Lifestyle-induced changes in alternative splicing patterns in mice
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Project description:Alternative splicing diversifies the cellular protein landscape but aberrant splicing is implicated in many diseases. We aimed to investigate to which extent mis-splicing contributes to insulin resistance as the causal defect of Type 2 Diabetes and whether diet- and exercise-based lifestyle interventions can reverse mis-splicing.
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