Transcription profiling of S. cerevisiae reveals transient transcriptional responses to stress are generated by opposing effects of mRNA production and degradation
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
SUBMITTER: Ophir Shalem
PROVIDER: E-GEOD-12222 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We subjected yeast to two stresses, oxidative stress, which under current settings induces a fast and transient response in mRNA abundance, and DNA damage, which triggers a slow enduring response. Using microarrays, we performed a transcriptional arrest experiment to measure genome-wide mRNA decay profiles under each condition. Genome-wide decay kinetics in each condition were compared to decay experiments that were performed in a reference condition (only transcription inhibition without an additional stress) to quantify changes in mRNA stability in each condition. We found condition-specific changes in mRNA decay rates and coordination between mRNA production and degradation. In the transient response, most induced genes were surprisingly destabilized, while repressed genes were somewhat stabilized, exhibiting counteraction between production and degradation. This strategy can reconcile high steady-state level with short response time among induced genes. In contrast, the stress that induces the slow response displays the more expected behavior, whereby most induced genes are stabilized, and repressed genes destabilized. Our results show genome-wide interplay between mRNA production and degradation, and that alternative modes of such interplay determine the kinetics of the transcriptome in response to stress. Experiment Overall Design: We used Affymetrix microarrays to measure the decay profiles of all genes following transcription inhibition in four separate experiments. In two reference experiments, only transcription inhibtion was applied. In two other experiments, an additional stress was applied prior to transcription inhibition: oxidative stress (0.3mM hydrogen peroxide) or DNA damage (0.1% methyl methanesulfonate).
2008-10-26 | E-GEOD-12221 | biostudies-arrayexpress
Project description:For each strain two time courses for mRNA abundance: Oxidative and MMS and two time courses for decay: reference decay and following oxidative stress We used Affymetrix microarrays to quantify changes in mRNA abundance following oxidative stress and DNA damage stress and also decay following transcription inhibition with and without oxidative stress. Each of the experiments were done for both strains 211 (wt) and 212 (mutant)
2011-07-29 | E-GEOD-26829 | biostudies-arrayexpress
Project description:We subjected yeast to two stresses, oxidative stress, which under current settings induces a fast and transient response in mRNA abundance, and DNA damage, which triggers a slow enduring response. Using microarrays we performed a conventional quantification of change in mRNA abundance. Experiment Overall Design: We used Affymetrix microarrays to quantify changes in mRNA abundance following oxidative stress (using hydrogen peroxide) and DNA damage stress (using methyl methanesulfonate) during a three-hour time course (0, 30 min, 60 min, 100 min, 140 min, 180 min).
2008-10-26 | E-GEOD-12220 | biostudies-arrayexpress
Project description:Investigation into the role of the S. pombe Fil1 transcription factor in multiple stress responses.
2020-11-18 | E-MTAB-8583 | biostudies-arrayexpress
Project description:A chromatin re-localization screen for the identification of Poly-ADP-ribosylation (PARylation)-dependent DNA repair factors.
2024-01-26 | PXD045229 | Pride
Project description:Maintenance of genetic integrity is essential for survival of all organisms. Activating transcription factor 3 (ATF3) is a member of the c-AMP response element binding (CREB)/ATF family of transcription factors, and is highly inducible by various stress conditions including DNA damage. However, downstream targets and molecular basis underlying pleiotropic effects of ATF3 on the cell fate have been largely unknown. To identify ATF3 targets in the human genome, we carried out chromatin immunoprecipitation-microarray (ChiP-on-chip) and knockdown-expression profiling analysis using two models where ATF3 was either transiently induced or constitutively expressed. We show that ATF3 binds to an unexpectedly large number of targets; 5,984 promoters in HCT116 cells treated with an alkylating agene methyl methanesulfonate (MMS) and 1,423 promoters in LNCaP cells constitutively expressing ATF3. Importantly, targets of MMS-induced ATF3 are highly enriched not only for CREB/ATF motifs but also for binding sites of several stress sensors including DDIT3/CHOP, Egr1, and c-Ets which are concomitantly induced by MMS. Stress-induced ATF3 affects broad but select biological processes including cell cycle, cell death, adhesion, biosynthesis, and receptor signaling pathways. In addition, ATF3 binds to as many as 40% of the p53 targets and preferentially enhances MMS-induced activation of proapoptotic genes such as DR4, DR5, and PUMA, consistent with the proapoptotic effect of ATF3. These data shed new light on the co-regulatory function of ATF3 in the stress-induced transcription factor network. The comprehensive list of genomic targets of ATF3 will facilitate further understanding the role of ATF3 in determining life and death of cells under both physiological and tumour-associated stress conditions. Maintenance of genetic integrity is fundamental to survival of all organisms. DNA damage can be caused by various agents in environment and elicits complex responses in the cell. ATF3 is one of the transcription factors activated by various stress conditions including DNA damage, and has been shown to have pleiotropic effects on life and death of cells depending on the context of experimental conditions. It has been largely unknown, however, which genes and pathways are regulated by stress-induced ATF3. Here we attempted to answer this question by chromatin immunoprecipitation-microarray analysis of downstream targets of ATF3. We show that ATF3 binds to an unexpectedly large number of promoters (nearly 6,000) in a human colorectal cancer cell lineHCT116 treated with an alkylating agent methyl methanesulfonate. Interestingly, the ATF3 targets are highly enriched for binding sites of other stress sensors shedding light on a transcriptional co-regulatory network of DNA damage response. We further show that ATF3 regulates expression of genes in select biological processes including cell cycle, cell death, adhesion, metabolism, signal transduction, and the p53 pathway. The comprehensive list of ATF3 targets provides new insight into a highly inter-connected network of stress-induced transcription factors around ATF3. ChIP-chip samples: Comparison of ATF3-IP and whole genome DNA (control) Gene expression samples: HCT116 cells pre-transfected with either control siRNA or ATF3 knockdown siRNA and stimulated by methyl methanesulfonate (MMS) for 0, 6, 12, and 24 hours
2010-10-01 | E-GEOD-18457 | biostudies-arrayexpress
Project description:Here we present the study on ChIP-chip mapping of the genomic binding sites for Sty1, Atf1, and the Atf1's binding partner Pcr1; the genome-wide transcriptional profiling of the atf1 and pcr1 strains in response to H2O2; and the phenotypic assessment of ~90 Atf1/Pcr1-bound or unbound genes for growth fitness under H2O2 conditions. ChIP-chip analysis shows that Atf1 and Pcr1 binding sites are overlapped in the genome and constitutively present before H2O2 stress. On the other hand, Sty1 recruitment primarily occurs at the Atf1/Pcr1 binding sites and is induced by H2O2. We found that Atf1/Pcr1 is clearly responsible for the high-level transcriptional response to H2O2. Furthermore, phenotypic assessment indicates that among the H2O2-induced genes, Atf1/Pcr1-bound genes exhibit a higher likelihood of functional requirement for growth fitness under the stress condition than the Atf1/Pcr1-unbound genes do. Notably, we found that the Atf1/Pcr1-bound genes regardless of their responsiveness to H2O2 show a high probability of requirement for growth fitness. . Expression level of genes in triplicates at 0min (without stress) is compared with that at 10, 30, 60, and 120min after stress treatment. ChIP-chip analyses is done for Atf1-HA, pcr1-HA, sty1-HA, Sty1-HA allele in the atf1D or pcr1D background without and with H2O2 (0.5mM for 30min).
2010-07-19 | E-GEOD-13053 | biostudies-arrayexpress
Project description:Technological advances now make gene expression analysis feasible in any sequenced organism, and new sequencing methods have greatly accelerated genome sequencing. Here we show that important insights into gene function are possible by comparing gene expression response to genetic and environmental perturbations between related species. We present a gene expression compendium designed for maximal gene expression variation in the sensu stricto yeast Saccharomyces bayanus. While many aspects of gene expression are conserved over the 20 million years of evolution separating S. bayanus from the model yeast S. cerevisiae, we observe regulatory changes, including in galactose metabolism and sporulation. The expression data also allows us to predict the biological roles of genes unique to S. bayanus, leading us to propose a role in oxidative stress response for a group of genes, and also to identify a regulatory network specific to this yeast. This dataset contains 53 experiments as follows: (experiment: number of datasets (number of arrays)) growth at different temperatures: 1 (3) heat shock: 4 (18) ammonium: 1 (6) cadmium: 1 (4) copper: 1 (6) lead: 1 (6) nickel: 1 (5) sulfite toxicity: 1 (6) zinc: 1 (6) ethanol toxicity: 1 (6) sorbitol: 1 (6) bleach: 1 (6) hydrogen peroxide: 3 (17) 2-deoxyglucose: 1 (6) hydroxyurea: 1 (6) lovastatin: 1 (4) MG-132: 1 (5) MMS: 1 (6) rapamycin: 1 (6) tunicamycin: 1 (6) zeocin: 1 (6) chronological aging: 3 (13) diauxic shift: 1 (6) galactose: 5 (38) glycerol: 1 (4) sucrose: 1 (4) auxotroph starvation: 1 (11) nutrient limited chemostat growth: 3 (7) mating type and ploidy: 1 (3) alpha factor: 1 (8) cell cycle: 1 (30) sporulation: 3 (18) strain backgrounds: 1 (4) cross progeny: 1 (22) Tn7 insertions: 1 (27) 555.11 and 670.20 knockout tetrads: 2 (8) Timecourse datasets: heat shock, ammonium, cadmium, copper, lead, nickel, sulfite toxicity, zinc, ethanol toxicity, sorbitol, bleach, hydrogen peroxide, 2-deoxyglucose, hydroxyurea, lovastatin, MG-132, MMS, rapamycin, tunicamycin, zeocin, chronological aging, diauxic shift, galactose, glycerol, sucrose, auxotroph starvation, alpha factor, cell cycle, sporulation Single timepoint datasets: growth at different temperatures, strain backgrounds, cross progeny, Tn7 insertions, nutrient limited chemostat growth, mating type and ploidy, 555.11 and 670.20 knockout tetrads Almost all samples were hybridized versus a common reference prepared from a mixture of RNA from Mat a, Matx, and Mata/x cells sampled in both exponential and stationary phase. Additionally, RNA from stress conditions was included: hydrogen peroxide treatment sampled at 10, 30 and 45 minutes, and heat shock from 25 to 37 degrees sampled at 10 and 30 minutes. Samples from the following datasets were not hybridized versus the common reference (reference used in parenthesis and in array annotations): cell cycle (asynchronous culture), constant temperatures (log phase culture), mating type and ploidy (log phase culture), diauxic shift (log phase culture), and strain backgrounds (log phase culture). Replicates and dye swaps were not used.
2010-05-16 | E-GEOD-16544 | biostudies-arrayexpress
Project description:Analysis of mRNA stability in S. cerevisiae in connection to hyperosmotic stress at different time points following mild hyperosmotic shock in Saccharomyces cerevisiae cells.
2009-01-22 | E-TABM-622 | biostudies-arrayexpress
Project description:Proteomic analysis was performed on the proximal tibia head from healhty and BCO-affected broiler (meat-type) chickens using Bruker Daltonics amaZon series Mass Spectrometer. This analysis was undertaken to identify key protein signature involved in BCO, a common cause of lameness.
2023-05-10 | PXD029085 | Pride