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Whole genome analysis of p38 SAPK-mediated gene expression upon stress

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE18320 | GEO | 2010/09/29

SECONDARY ACCESSION(S): PRJNA117973

REPOSITORIES: GEO

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Whole genome analysis of p38 SAPK-mediated gene expression upon stress

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

p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress

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

Effect of p38 SAPK activation on HeLa cells

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.

2019-04-16 | GSE117996 | GEO

p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress

Project description:p38 SAPK and SKIIP induced changes in alternative splicing patterns upon osmostress

| PRJNA482978 | ENA

Effect of p38 SAPK activation on HeLa cells

Project description:Effect of p38 SAPK activation on HeLa cells

| PRJNA483952 | ENA

ZAK activation on colliding ribosomes triggers SAPK signaling pathways to regulate cell fate

Project description:Problems arising during translation of mRNAs lead to ribosome stalling and collisions with trailing ribosomes. These collisions are known to trigger a series of events including degradation of the stalled nascent polypeptide, decay of the problematic mRNAs, and ribosome rescue. However, the systemic cellular response of ribosome collision has not been explored. Here, we uncover a novel function for ribosome collisions in signal transduction. Using multiple translation elongation inhibitors and cellular stress conditions, we show that ribosome collisions activate both the SAPK (Stress Activated Protein Kinase) and GCN2-mediated cellular stress response pathways that lead to apoptosis and the integrated stress response (ISR), respectively. We further show that the MAPKKK ZAK functions as the sentinel for ribosome collisions, and ZAK is required for activation of both SAPKs p38/JNK and GCN2 signaling pathways. Selective ribosome profiling and biochemistry demonstrate that ZAK preferentially associates with the minimal unit of colliding ribosomes, the disome, inducing ZAK phosphorylation. While ZAK associates with elongating ribosomes under non-stressed conditions, activation of ZAK is specifically trigger by colliding ribosomes. Together, these results provide new insights into how perturbation of translational homeostasis, as read-out by colliding ribosomes, regulates cell fate.

2020-08-18 | GSE141459 | GEO

Hog1 bypasses stress-mediated down-regulation of transcription by PolII redistribution and chromatin remodeling

Project description:Cells are subjected to dramatic changes on gene expression upon environmental changes. Stress causes a general down-regulation of gene expression together with the induction of a set of stress-responsive genes. Genome wide localisation studies showed major changes on Pol II localisation towards stress-responsive genes in contrast to housekeeping genes. Pol II relocalisation requires of the Hog1 SAPK, which also associates at stress-responsive loci. Chromatin structure was not significantly altered upon stress except for those genes that displayed Hog1 association. Together, Hog1 serves to bypass the general down-regulation of gene expression by targeting RNA Pol II machinery and inducing chromatin remodeling at stress-responsive loci. Hog1 and Pol II ChIP-Seq and Mnase-Seq experiments in both strains WT and Hog1 mutant, for 2 conditions: Exposed and not exposed to osmostress

2012-10-30 | E-GEOD-41494 | biostudies-arrayexpress

Mus musculus

Project description:Whole genome analysis of p38 SAPK-mediated gene expression upon stress

| PRJNA117973 | ENA

Proinflammatory Responses of Human Airway Cells to Ricin Involve Stress-Activated Protein Kinases and NF-κB

Project description:Ricin is a potential bioweapon because of its toxicity, availability, and ease of production. When delivered to the lungs, ricin causes severe pulmonary damage with symptoms that are similar to those observed in acute lung injury and adult respiratory distress syndrome. The airway epithelium plays an important role in the pathogenesis of many lung diseases, but its role in ricin intoxication has not been elucidated. Exposure of cultured primary human airway epithelial cells to ricin resulted in the activation of stress-activated protein kinases (SAPKs) and NF-κB and in the increased expression of multiple proinflammatory molecules. Among the genes upregulated by ricin and identified by microarray analysis were those associated with transcription, nucleosome assembly, inflammation, and response to stress. Sequence analysis of the promoters of these genes identified NF-κB as one of the transcription factors whose binding sites were over-represented. Although airway cells secrete TNF-α in response to ricin, blocking TNF-α did not prevent ricin-induced activation of NF-κB. Inhibition of p38 MAPK by a chemical inhibitor and NF-κB by short interfering RNA resulted in a marked reduction in the expression of proinflammatory genes, demonstrating the importance of these two pathways in ricin intoxication. Therefore, the p38 MAPK and NF-κB pathways are potential therapeutic targets for reducing the inflammatory consequences of ricin poisoning. Keywords: Comparative genomic hybridization

2007-05-22 | GSE7845 | GEO

Differential Responses of Plasmacytoid Dendritic Cells to Influenza and Distinct Viral Pathogens

Project description:Plasmacytoid dendritic cells (pDCs) are key components of the innate immune response that are capable of synthesizing and rapidly releasing vast amounts of type I interferons (IFNs), particularly IFN-alpha. Here we investigated whether pDCs, often regarded as a mere source of IFN, discriminate between various functionally discrete stimuli and to what extent this reflects differences in pDC responses other than IFN-alpha release. To examine the ability of pDCs to differentially respond to various doses of intact and infectious HIV, hepatitis C virus, and H1N1 influenza virus, whole-genome gene expression analysis, enzyme-linked immunosorbent assays, and flow cytometry were used to investigate pDC responses at the transcriptional, protein, and cellular levels. Our data demonstrate that pDCs respond differentially to various viral stimuli with significant changes in gene expression, including those involved in pDC activation, migration, viral endocytosis, survival, or apoptosis. In some cases, the expression of these genes was induced even at levels comparable to that of IFN-alpha. Interestingly, we also found that depending on the viral entity and the viral titer used for stimulation, induction of IFN-alpha gene expression and the actual release of IFN-alpha are not necessarily temporally coordinated. In addition, our data suggest that high-titer influenza A (H1N1) virus infection can stimulate rapid pDC apoptosis.

2014-07-28 | GSE59837 | GEO

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