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

ABSTRACT: 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

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Francesc Posas

PROVIDER: E-GEOD-41494 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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.

2012-10-30 | GSE41494 | GEO

Hog1 controls global reallocation of RNA Pol II upon osmotic shock

Project description:When challenged with osmotic shock, S. cerevisiae induces hundreds of genes, despite a global reduction in transcriptional capacity. The mechanisms that regulate this rapid reallocation of transcriptional resources are not known. Here we show that redistribution of RNA Pol II upon stress requires the stress-responsive MAP kinase Hog1. We find that Hog1 and RNA Pol II co-localize to open reading frames that bypass global transcriptional repression, and that these targets are specified by two osmotic stress-responsive transcription factors. The combination of reduced global transcription with a gene-specific override mechanism allows cells to rapidly switch their transcriptional program in response to stress. ChIP-sequencing of S. cervisiae RNA Pol II, Hog1, Sko1 and Hot1 Processed data file descriptions: ORFcounts.txt: table of summed ChIP-seq reads that align to each ORF (normalized by reads per kilobase per million) promoter_counts.txt: table of summed ChIP-seq reads that align to each promoter (1kb upstream, normalized by reads per kilobase per million) downstream_counts.txt: table of summed ChIP-seq reads that align 3' regions (50-500 bp downstream, normalized by reads per kilobase per million) Sko1_peak_list.txt: table of peaks found by PeakSeq Hot1_peak_list.txt: table of peaks found by PeakSeq

2012-07-15 | E-GEOD-38208 | biostudies-arrayexpress

Hog1 controls global reallocation of RNA Pol II upon osmotic shock

2012-07-15 | GSE38208 | GEO

FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (HTS)

Project description:We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate (CPA), mifepristone (RU486) and bicalutamide (Bica) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies. Examination of AR and GR binding sites in LNCaP-1F5 and VCaP cells in presence of DHT and Dex respectively. Further analysis of AR binding sites in LNCaP-1F5 cells treated with partial agonist/antagonists, CPA, RU486 and Bica. Additionally RNA Pol II mapping is performed in cells treated with DHT and Dex.

2013-02-05 | E-GEOD-39879 | biostudies-arrayexpress

RNA polymerase II pausing downstream of core histone genes is different from genes producing polyadenylated transcripts

Project description:Recent genome-wide chromatin immunoprecipitation coupled high throughput sequencing (ChIP-seq) analyses performed in various eukaryotic organisms, analysed RNA Polymerase II (Pol II) pausing around the transcription start sites of genes. In this study we have further investigated genome-wide binding of Pol II downstream of the 3' end of the annotated genes (EAGs) by ChIP-seq in human cells. At almost all expressed genes we observed Pol II occupancy downstream of the EAGs suggesting that Pol II pausing 3' from the transcription units is a rather common phenomenon. Downstream of EAGs Pol II transcripts can also be detected by global run-on and sequencing, suggesting the presence of functionally active Pol II. Based on Pol II occupancy downstream of EAGs we could distinguish distinct clusters of Pol II pause patterns. On core histone genes, coding for non-polyadenylated transcripts, Pol II occupancy is quickly dropping after the EAG. In contrast, on genes, whose transcripts undergo polyA tail addition [poly(A)+], Pol II occupancy downstream of the EAGs can be detected up to 4-6 kb. Inhibition of polyadenylation significantly increased Pol II occupancy downstream of EAGs at poly(A)+ genes, but not at the EAGs of core histone genes. The differential genome-wide Pol II occupancy profiles 3' of the EAGs have also been confirmed in mouse embryonic stem (mES) cells, indicating that Pol II pauses genome-wide downstream of the EAGs in mammalian cells. Moreover, in mES cells the sharp drop of Pol II signal at the EAG of core histone genes seems to be independent of the phosphorylation status of the C-terminal domain of the large subunit of Pol II. Thus, our study uncovers a potential link between different mRNA 3' end processing mechanisms and consequent Pol II transcription termination processes. Examination of RNA Polymerase II in MCF-7 cell line

2012-06-15 | E-GEOD-34001 | biostudies-arrayexpress

CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing

Project description:This SuperSeries is composed of the following subset Series: GSE31485: CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [ChIP-Seq] GSE31486: CTCF promotes RNA pol II pausing and links DNA methylation to alternative splicing [RNA-Seq] Refer to individual Series

2011-10-05 | E-GEOD-31278 | biostudies-arrayexpress

Rapid transcription of arc/arg3.1 and other very fast immediate early genes in response to neuronal activity is mediated by a stalled RNA polymerase II mechanism

Project description:Transcription of immediate early genes (IEGs) in neurons is exquisitely sensitive to neuronal activity, but the mechanism underlying the earliest of these transcription events is largely unknown. Here we demonstrate that very fast IEGs (VF-IEGs) such as arc/arg3.1 are poised for rapid transcription by the stalling of RNA Polymerase II (Pol II) just downstream of the transcription start site. RNAi-depletion of two subunits of Negative Elongation Factor, a mediator of Pol II stalling, reduces the Pol II occupancy of the arc promoter and compromises the rapid induction of arc and other VF-IEGs. In contrast, reduction of Pol II stalling did not prevent expression of fast IEGs (F-IEGs). These F-IEGs are expressed with comparatively slower kinetics and largely lack promoter proximal Pol II stalling. Taken together, our data strongly indicate that very fast kinetics of neuronal IEG expression require poised Pol II and suggest a role for this mechanism in transcription-dependent learning and memory. Examination of Pol II bindnig genome-wide in rat neurons

2011-05-24 | E-GEOD-22878 | biostudies-arrayexpress

Whole-genome landscape of histone H2AX and M-NM-3-H2AX

Project description:Phosphorylation of the histone variant H2AX forms M-NM-3-H2AX that marks DNA double-strand break (DSB). Here we generated the sequencing-based maps of H2AX and M-NM-3-H2AX positioning in resting and proliferating cells before and after ionizing irradiation. Genome-wide locations of possible endogenous and exogenous DSBs were identified based on M-NM-3-H2AX distribution in dividing cancer cells without irradiation and that in resting cells upon irradiation, respectively. M-NM-3-H2AX-enriched regions of endogenous origin in replicating cells included telomeres and active transcription start sites, apparently reflecting replication- and transcription-mediated stress during rapid cell division. Surprisingly, H2AX itself, prior to phosphorylation, was specifically located at these endogenous hotspots. This phenomenon was only observed in dividing cancer cells but not in resting cells. Endogenous H2AX was concentrated on the transcription start site of actively transcribed genes but was irrelevant to pausing of RNA polymerase II (pol II), which precisely coincided with M-NM-3-H2AX of endogenous origin. M-NM-3-H2AX enrichment upon irradiation also coincided with actively transcribed regions, but unlike endogenous M-NM-3-H2AX, it extended into the gene body and was not specifically concentrated on the pausing site of pol II. Subtelomeres were not responsive to external DNA damage. Our findings provide insight into DNA repair programs of cancer and may have implications for cancer therapy. Profiles of H2AX and gamma-H2AX in normal resting and cancer T cells with and without ionizing irradiation.

2012-04-03 | E-GEOD-25577 | biostudies-arrayexpress

CX-MS of TFIIH and Def1 complex

Project description:The DNA damage response is an essential process for the survival of living cells. In a subset of stress-responsive genes in humans,Elongin controls transcription in response to multiple stimuli, such as DNA damage, oxidative stress, and heat shock. Yeast Elongin (Ela1-Elc1), along with Def1, is known to facilitate ubiquitylation and degradation of RNA polymerase II (pol II) in response tomultiple stimuli, yet transcription activity has not been examined. We have found that Def1 copurifies from yeast whole-cell extract with TFIIH,the largest general transcription factor required for transcription initiation and nucleotide excision repair. The addition of recombinant Def1 and Ela1-Elc1 enhanced transcription initiation in an in vitro reconstituted system including pol II, the general transcription factors, and TFIIS. Def1 also enhanced transcription restart from TFIIS-induced cleavage in a pol II transcribing complex. In the Δdef1 strain, heat shock genes were misregulated, indicating that Def1 is required for induction of some stress-responsive genes in yeast. Taken together, our results extend the understanding of the molecular mechanism of transcription regulation on cellular stress and reveal functional similarities to the mammalian system.

2018-10-22 | PXD008223 | Pride

Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

Project description:H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with PPARβ/δ agonist (GW501516 100nM) and/or hypoxia (1%O2) for 24hours, then H3K27ac, PPARβ/δ and Pol II binding regions were identified. Normoxia and DMSO was used as a control condition. HUVECs were used within the first 6 passages.

2014-03-06 | E-GEOD-50144 | biostudies-arrayexpress

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