Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA118787 | ENA |
REPOSITORIES: ENA
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Project description:Cells respond to stress and starvation by adjusting their growth rate and enacting stress defense programs. In eukaryotes this involves inactivation of TORC1, which in turn triggers downregulation of ribosome and protein synthesis genes and upregulation of stress response genes. Here we report that the highly conserved inositol pyrophosphate second messengers (including 1-PP-IP5, 5-PP-IP4, and 5-PP-IP5) are also critical regulators of cell growth and the general stress response, acting in parallel to the TORC1 pathway to control the activity of the class I HDAC Rpd3L. In fact, yeast cells that cannot synthesize any of the PP-IPs mount little to no transcriptional response in osmotic, heat, or oxidative stress. Furthermore, PP-IP dependent regulation of Rpd3L occurs independently of the role individual PP-IPs (such as 5-PP-IP5) play in activating specialized stress/starvation response pathways. Thus, the PP-IP second messengers simultaneously activate and tune the global response to stress and starvation signals. 2-condition experiments. Includes the responses of wild-type (ACY 044) and mutant yeast strains (all are W303 background) to log growth and stress conditions. This series of microarrays were performed on null mutants of various genes in the inositol pyrophosphate synthesis pathway, including several members of the Rpd3L histone deacetylase complex. All mutants were made in W303 strain, MatA yeast, using standard techniques (homologous recombination). Several stress conditions were tested, including heat-shock, oxidative (H2O2), and osmotic stress (0.375M KCl). Cells in mid-log growth were subjected to stress for 20 minutes. In one instance the TOR inhibitor rapamycin was added to determine whether PP-IPs act above/at or below TORC1 in activating the ESR. Taken together, these microarrays show the role of the inositol pyrophosphate synthesis pathway in activating the ESR in stress.
2013-03-22 | E-GEOD-45370 | biostudies-arrayexpress
Project description:Cells respond to stress and starvation by adjusting their growth rate and enacting stress defense programs. In eukaryotes this involves inactivation of TORC1, which in turn triggers downregulation of ribosome and protein synthesis genes and upregulation of stress response genes. Here we report that the highly conserved inositol pyrophosphate second messengers (including 1-PP-IP5, 5-PP-IP4, and 5-PP-IP5) are also critical regulators of cell growth and the general stress response, acting in parallel to the TORC1 pathway to control the activity of the class I HDAC Rpd3L. In fact, yeast cells that cannot synthesize any of the PP-IPs mount little to no transcriptional response in osmotic, heat, or oxidative stress. Furthermore, PP-IP dependent regulation of Rpd3L occurs independently of the role individual PP-IPs (such as 5-PP-IP5) play in activating specialized stress/starvation response pathways. Thus, the PP-IP second messengers simultaneously activate and tune the global response to stress and starvation signals.
2013-03-22 | GSE45370 | GEO
Project description:Samples GSM206658-GSM206693: Acquired Stress resistance in S. cerevisiae: NaCl primary and H2O2 secondary Transcriptional timecourses of yeast cells exposed to 0.7M NaCl alone, 0.5mM H2O2 alone, or 0.5mM H2O2 following 0.7M NaCl, all compared to an unstressed sample. Repeated using msn2∆ strain. Samples GSM291156-GSM291196: Transcriptional response to stress in strains lacking MSN2 and/or MSN4 Transcriptional timecourses of yeast cells (WT, msn2∆, msn4∆, or msn2∆msn4∆) exposed to 0.7M NaCl for 45 minutes or 30-37˚C Heat Shift for 15 min compared to an unstressed sample of the same strain. Keywords: Stress Response
2008-09-05 | GSE8335 | GEO
Project description:Disomic yeast response to heat shock
| PRJNA172729 | ENA
Project description:Gene expression regulation in response to heat stress in different yeast strains
| PRJNA119447 | ENA
Project description:Transcriptional memory is critical for the faster reactivation of necessary genes upon environmental changes and requires that the genes were previously in an active state. However, whether transcriptional repression also displays “memory” of the prior transcriptionally inactive state remains unknown. In this study, we show that transcriptional repression of approximately 540 genes in yeast occurs much more rapidly if the genes have been previously repressed during carbon source shifts. This novel transcriptional response has been termed transcriptional repression memory(TREM). Interestingly, Rpd3L histone deacetylase (HDAC), targeted to active promoters induces TREM. Mutants for Rpd3L exhibit increased acetylation at active promoters and delay TREM and RNA PolII dissociation significantly. Surprisingly, the interaction between H3K4me3 and Rpd3L via the Pho23 PHD finger is sufficient to induce histone deacetylation and TREM by Rpd3L. Therefore, we propose that an active mark, H3K4me3 enriched at promoters, instructs Rpd3L HDAC to induce histone deacetylation and TREM.
2018-10-23 | E-MTAB-6551 | biostudies-arrayexpress
Project description:DNA replication forks that are stalled by DNA damage activate an S phase checkpoint that prevents irreversible fork arrest and cell death. The increased cell death caused by DNA damage in budding yeast cells lacking the Rad53 checkpoint protein kinase is partially suppressed by deletion of the EXO1 gene. Here,we identified that loss of the histone deacetylase complex Rpd3L promotes survival of rad53∆ cells exposed to DNA damaging agents. From epistasis analysis, we show that this suppression operates in a separate pathway from the previously described suppression by deletion of EXO1.
2019-02-27 | GSE113869 | GEO