Structure and Function of a Transcriptional Network Activated by Hog1
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ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE12270 | GEO | 2008/07/29
SECONDARY ACCESSION(S): PRJNA113655
REPOSITORIES: GEO
Similar Datasets
Project description:Cells regulate gene expression using a complex network of signaling pathways, transcription factors and promoters. To gain insight into the structure and function of these networks we analyzed gene expression in single and multiple mutant strains to build a quantitative model of the Hog1 MAPK-dependent osmotic stress response in budding yeast. Our model reveals that the Hog1 and general stress (Msn2/4) pathways interact, at both the signaling and promoter level, to integrate information and create a context-dependent response. Keywords: Stress response network analysis using genetically modified cells 85 samples were used to dissect the structure and function of the Hog1 network (Critical Samples measured in triplicate). The overall strategy was to double mutant or epistasis analysis to break down the influence that genes in the Hog1 network have on each other and the genome-wide stress response. This was done by comparing the expression in strains with different combinations of genes deleted and fitting the data to quantitative models. See Capaldi et. al. Nature Genetics 2008 for details.
2008-07-29 | E-GEOD-12270 | biostudies-arrayexpress
Project description:In budding yeast, this signaling pathway— the high-osmolarity glycerol (HOG) response —culminates in dual phosphorylation and nuclear translocation of the MAPK, Hog1 (ortholog of mammalian p38/SAPK). Induction of at least 50 genes requires nuclear Hog1, implying that transcriptional up-regulation is necessary to cope with hyperosmotic stress. Contrary to this expectation, we found that cells lacking the karyopherin (Nmd5) required for Hog1 nuclear import or in which Hog1 was permanently anchored at the plasma membrane(HOG1-CCAAX) (or both) withstood hyperosmotic challenge by three different solutes (1 M sorbitol, KCl or NaCl). In cells where activated Hog1 is excluded from the nucleus, there was little change in transcriptional program after exposure to hyperosmotic shock (comparable to hog1∆ cells), as judged by examining several diagnostic mRNAs and by global transcript measurements using microarrays. Systematic genetic analysis ruled out the need for any transcription factor known to be influenced by Hog1 (Hot1, Msn2, Msn4, Sko1 and Smp1). Keywords: Time course of stress response gene expression array
2008-06-01 | GSE8703 | GEO
Project description:We did transcription profiling on the effect of hog1 deletion, gene involved in cell osmotic stress and cell wall stress response Keywords: cell wall stress response
2008-09-06 | GSE9931 | GEO
Project description:Epigenetic information is able to interact with the cellular environment and therefore it could be especially useful for reprogramming gene expression in response to a physiological perturbation. In fact, genes induced or repressed by osmotic stress undergo significant changes in the levels of various histone modifications, especially the acetylation levels of histone H3. Exposure of yeast to high osmolarity results in the activation of p38-related SAPK, Hog1, which plays a central role in the control of gene expression. Therefore, two types of mechanisms converge in gene regulation by stress: that of the epigenetic signals and that of the trans-acting protein factor. We have evaluated the connection between the presence of Hog1 and the changes on acetylation of histone H3 in stress-regulated genes. Furthermore, we asked which enzymatic activities are involved in the changes produced in the acetylation of H3 linked to gene activation by osmotic stress. We have demonstrated that increase of acetylation of lysines 9 and 14 of H3 produced on induced genes during stress positively correlates between them and are largely dependent on Hog1 at genome-wide level. Conversely, decrease in acetylation on repressed genes was not dependent on Hog1. However, the absence of Hog1 produces different and even opposite effects on the induction and acetylation of H3 of each gene, which suggests that Hog1 influences both processes through different mechanisms. Additionally, we found that in genes up-regulated during osmotic stress in a Msn2/Msn4-independent manner, the state of acetylation of lysine 9 of H3 was altered in strains deficient in Nut1 HAT and Hos1 HDAC; meanwhile for Msn2/Msn4-dependent induced genes H3k9 acetylation varies in strains deficient in Sas2 HAT and Rpd3 HDAC. During induction by osmotic stress at least two different mechanism act on H3k9 acetylation of two differentiated set of induced genes, one of them would act through Nut1/Hos1, while the other through Sas2/Rpd3. The results presented here show new and unexpected participants in the process of the regulation of gene in response to environmental perturbations.
2019-07-01 | GSE127742 | GEO
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.
2012-07-15 | GSE38208 | GEO
Project description:The stress-activated protein kinase Hog1 is best known for its role in osmotic stress but is also activated by a variety of mechanistically distinct environmental stressors including heat shock, ER stress, and arsenic. In the osmotic stress response, the signal is sensed upstream and relayed to Hog1 via a kinase cascade. Here we identify a novel mode of Hog1 function whereby Hog1 senses arsenic though direct physical interaction requiring three conserved cysteine residues located adjacent to the catalytic loop. These residues are essential for Hog1's role in protecting against arsenic, but completely dispensable for osmotic stress, and mediate Hog1's cellular localization upon arsenic exposure. Hog1 in turn regulates arsenic detoxification by phosphorylating the transcription factor Yap8, promoting its nuclear localization, and stimulating transcription of its only known targets, Arr2 and Arr3, which promote arsenic efflux. Arsenic binding was also observed with the related human kinases Erk1 and Erk2, suggesting that this may be a conserved aspect of this kinase family. These data provide a mechanistic basis for understanding how stress-activated kinases can sense individual threats and carry out highly specific adaptive responses.
2019-12-04 | PXD015325 | Pride
Project description:In budding yeast, this signaling pathway— the high-osmolarity glycerol (HOG) response —culminates in dual phosphorylation and nuclear translocation of the MAPK, Hog1 (ortholog of mammalian p38/SAPK). Induction of at least 50 genes requires nuclear Hog1, implying that transcriptional up-regulation is necessary to cope with hyperosmotic stress. Contrary to this expectation, we found that cells lacking the karyopherin (Nmd5) required for Hog1 nuclear import or in which Hog1 was permanently anchored at the plasma membrane(HOG1-CCAAX) (or both) withstood hyperosmotic challenge by three different solutes (1 M sorbitol, KCl or NaCl). In cells where activated Hog1 is excluded from the nucleus, there was little change in transcriptional program after exposure to hyperosmotic shock (comparable to hog1∆ cells), as judged by examining several diagnostic mRNAs and by global transcript measurements using microarrays. Systematic genetic analysis ruled out the need for any transcription factor known to be influenced by Hog1 (Hot1, Msn2, Msn4, Sko1 and Smp1). Keywords: Time course of stress response gene expression array The transcriptomes' of HOG1-GFP, hog1del, and HOG1-CCAAX strains before and after 60 min hyperosmotic shock with 1M sorbitol at 25C were compared. Three biological replicates were done, with the first biological replicate done in technical triplicate, and the final two biological replicates beind done in technical duplicate by in slide duplication of features. Several supplementary files attached to the Series are summarized below: GSE8703 B1, B2, B3 Tscombined_matrix files show the averages of the technical replicates for each biological replicate. GSE8703 B1, B2, B3 norm_to_0_matrix files show the fold change over the time course (log2 time 60 - log2 time 0) for each of the three strains in each biological replicate. GSE8703 Figure_S6 shows the 30 genes with the most significant difference between the HOG1-GFP strain and the hog1del strain as determined by SAM. Genes were identified as: >3 fold induction in HOG1-GFP over 60 minute hyperosmotic shock and <3 fold induction in hog1del over 60 minute hyperosmotic shock.
2008-06-01 | E-GEOD-8703 | biostudies-arrayexpress
Project description:mRNA amount (RA) analysis of W303 hog1 mutant yeast strain growing in exponential phase in YPD subjected to osmotic stress Keywords: Time course
2009-04-23 | GSE13099 | GEO
Project description:Transcription rate (TR) analysis of W303 hog1 mutant yeast strain growing in exponential phase in YPD subjected to osmotic stress Keywords: Time course
2009-04-23 | GSE13098 | GEO
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