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Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila (ChIP-Seq)

ABSTRACT: Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila (ChIP-Seq)

PROVIDER: PRJNA911284 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22689950.fastq.gz	Fastqsanger.gz
	SRR22689951.fastq.gz	Fastqsanger.gz
	SRR22689952.fastq.gz	Fastqsanger.gz
	SRR22689953.fastq.gz	Fastqsanger.gz
	SRR22689954.fastq.gz	Fastqsanger.gz

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Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila

Project description:Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila

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Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila (RNA-Seq)

Project description:Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila (RNA-Seq)

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Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila (RNA-Seq)

Project description:p38 mitogen-activated protein kinases play fundamental roles in the regulation of the cellular response to environmental stress. p38 is known to regulate translation, mRNA processing and stability, and transcription. The transcriptional response mediated by phosphorylated p38 (P-p38) to extracellular stimuli, such as growth factors, cytokines and different environmental agents, has been thoroughly analysed in a variety of tissues and organisms. However, the genomic localisation of P-p38 is poorly understood. Here, we analysed the chromatin binding of activated P-p38 and the transcriptional response triggered by reactive oxygen species (ROS) in Drosophila S2 cells. We found that P-p38 is already bound to chromatin in basal conditions and relocates in the genome after exposure to high levels of ROS. The distribution pattern of P-p38 suggests that it is involved in the activation and repression of transcription in S2 cells, mainly regulating house-keeping functions.

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Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila (ChIP-Seq)

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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

Role of nuclear p38 in the transcriptional response to oxidative stress in Drosophila

Project description:This SuperSeries is composed of the SubSeries listed below.

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The role of Calment in Drosophila longevity and oxidative stress resistance

Project description:The aim of this study is to gain insights into how Calment/CG3036 affects lifespan and oxidative stress resistance in Drosophila females. Here we perform a microarray analysis in isogenized Calment1/4 females and CanS controls

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p38 MAPK-dependent phosphorylation of TFEB promotes monocyte-to-macrophage differentiation

Project description:In addition to the role in lysosomal biogenesis and autophagy, TFEB has been described to participate in the control of inflammation and host defense against pathogen infection The activation of TFEB in toll-like receptor-induced or bacteria exposed macrophages is regulated by a mechanism independent of mTORC1 inactivation, suggesting that other protein kinases may participate in the regulation of TFEB function during macrophage activation In this study, we identified a novel role of p38 MAPK in TFEB regulation. We showed p38-dependent TFEB phosphorylation at serine 401 (S401) in response to a variety of stress conditions, including oxidative stress, UVC irradiation, growth factors, and lipopolysaccharide (LPS) treatment. Furthermore, inhibition of S401 phosphorylation during PMA-induced monocyte differentiation prevented TFEB nuclear accumulation and resulted in reduced expression of multiple immune genes. TFEB-S401A expressing M0 macrophages also failed to efficiently polarize into M1 inflammatory macrophages, showing defective upregulation of cytokines and chemokines, as well as reduced inflammasome activation. We conclude that TFEB is a target of the p38 signaling pathway that is required for monocyte/macrophage differentiation and function.

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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.

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Project description:Role of BmoR in Bacteroides fragilis response to oxidative stress

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