Saccharomyces cerevisiae
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ABSTRACT:
PROVIDER: PRJNA90773 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Time-course analyses of the modifications of the yeast gene expression program which immediately follows addition of the antimitotic drug benomyl. Parallel experiments were conducted in different genetic contexts using strains deleted in the Yap1 and Pdr1 genes. Keywords: other
2004-09-06 | GSE1617 | GEO
Project description:Time-course analyses of the modifications of the yeast gene expression program which immediately follows addition of the antimitotic drug benomyl. Parallel experiments were conducted in different genetic contexts using strains deleted in the Yap1 and Pdr1 genes.
2004-09-06 | E-GEOD-1617 | biostudies-arrayexpress
Project description:Yeast is a powerful model system for studying the action of small molecule therapeutics. An important limitation has been low efficacy of many small molecules in yeast due to limited intracellular drug accumulation. We used the DNA binding domain of the pleiotropic drug resistance regulator Pdr1 fused in-frame to transcription repressors to repress Pdr1 regulated genes. Expression of these regulators conferred dominant enhancement of drug sensitivity and led to greatly diminished levels of Pdr1p regulated transcripts, including the yeast p-glycoprotein homologue Pdr5. Enhanced sensitivity was seen for a wide range of small molecules. Biochemical measurements demonstrated enhanced accumulation of rhodamine in yeast cells carrying the chimeras. These repressors of Pdr1p regulated transcripts can be introduced into large collections of strains such as the S. cerevisiae deletion set, and enhance the utility of yeast for studying drug action and for mechanism-based drug discovery. Keywords: Comparison of genetic variants
2007-06-29 | GSE8326 | GEO
Project description:Growth assay in the presence of a toxic chemical (sr7575) that uses the barcoded collections of yeast gene deletions (haploid, diploid, DamP) to identify deletion strains that are hypersensitive to the drug.
2015-12-09 | GSE60934 | GEO
Project description:Yap1 targets under normal and cobalt surplus growth conditions. Yeast strains (wild-type and yap1 mutant, BY4742 background) were grown until early log-phase and either untreated or exposed to 2mM of CoSO4 for 60 min. Changes in the transcriptome of yap1 mutant cells were then analyzed.
2014-01-01 | E-MEXP-3874 | biostudies-arrayexpress
Project description:Growth assay in the presence of a toxic chemical that uses the barcoded collections of yeast gene deletions (haploid, diploid, DamP) to identify deletion strains that are hypersensitive to the drug.
2019-12-31 | GSE125353 | GEO
Project description:Yeast is a powerful model system for studying the action of small molecule therapeutics. An important limitation has been low efficacy of many small molecules in yeast due to limited intracellular drug accumulation. We used the DNA binding domain of the pleiotropic drug resistance regulator Pdr1 fused in-frame to transcription repressors to repress Pdr1 regulated genes. Expression of these regulators conferred dominant enhancement of drug sensitivity and led to greatly diminished levels of Pdr1p regulated transcripts, including the yeast p-glycoprotein homologue Pdr5. Enhanced sensitivity was seen for a wide range of small molecules. Biochemical measurements demonstrated enhanced accumulation of rhodamine in yeast cells carrying the chimeras. These repressors of Pdr1p regulated transcripts can be introduced into large collections of strains such as the S. cerevisiae deletion set, and enhance the utility of yeast for studying drug action and for mechanism-based drug discovery. Experiment Overall Design: We determined the profiles of gene expression in yeast strains expressing dominant-negative Pdr1-fusion transcription factors. Yeast strains expressing different Pdr1-fusion repressors were analyzed by extracting total RNA and hybridization to Affymetrix GeneChip YG-s98 microarrays
2008-06-16 | E-GEOD-8326 | biostudies-arrayexpress
Project description:Growth assay in the presence of a toxic chemical (sr7575) that uses the barcoded collections of yeast gene deletions (haploid, diploid, DamP) to identify deletion strains that are hypersensitive to the drug. Two-condition experiment â growth of a pool of strains in the presence or absence of the drug. Two independent biological replicates for each collection (haploids - homozygous and diploids â heterozigous). Data for the article: Shriya Raj, Karthik Krishnan, David S Askew, Olivier Helynck, Peggy Suzanne, Aureslien Lesnard, Sylvain Rault, Ute Zeidler, Christophe d'Enfert, Jean-Paul Latgé, Hélène Munier-Lehmann and Cosmin Saveanu. Toxicity of a novel antifungal compound is modulated by ERAD components. Antimicrobial Agents and Chemotherapy.
2015-12-09 | E-GEOD-60934 | biostudies-arrayexpress
Project description:Arsenic metalloid is a double-edge sword. On the one hand it is a very toxic and powerful carcinogen, and on the other it has been successfully used in the treatment of acute promyelocytic leukemia. In order to prevent the deleterious effects caused by arsenic compounds, almost all living organisms have developed mechanisms to eliminate it. In this study genome-wide response of S. cerevisiae to arsenic shows that this metal interferes with genes involved in the iron homeostasis including those encoding proteins that function in iron uptake, incorporation into Fe–S clusters, and more. In addition our data indicate that Yap1 transcriptionally controls the iron homeostasis regulator AFT2 as well as its direct target, MRS4. Most importantly in response to arsenate exposure Yap1 strongly regulates the expression of several genes involved in the Fe-S proteins biosynthesis, namely NBP35 and YFH1. Interestingly mRNA levels encoding Fet3, Ferro-O2-oxidoreductase required for high-affinity iron uptake, are drastically destabilized upon arsenic exposure. Such destabilization is due to the 5’ to 3’ exonuclease Xrn1 localized in the P Bodies. Moreover FET3 mRNA decay is not mediated by Cth2 and is independent on the formation of ROS responsible for the toxic effects of arsenic compounds. Strikingly, in presence of arsenate fet3 mutant shows resistance over the wild-type which leads us to suggest that Fet3 has a role in arsenic toxicity. Unexpectedly arsenic treatment seems to activate the non-reductive iron uptake in order to maintain the cellular iron homeostasis. Furthermore our genetic, biochemical, and physiological analysis demonstrate that aft1 mutant is sensitive to arsenic compounds and such phenotype is reversible upon addition of iron. We also show that arsenic exposure induces iron deficiency in aft1 mutant. In conclusion this work shows for the first time that arsenic, a chemotherapy drug used to treat a specific type of acute promyelocytic leukemia (APL), disrupts iron homeostasis and our results suggest that this disruption is independent on ROS generation. Finally we provide preliminary data confirming that such disruption also takes place in mammalian cells, an observation that can be very relevant in term of clinical applications. yap1yap8 mutant cells independently transformed with pRS416 and YcpLac111, YcpLac111-YAP1, or pRS416-YAP8 were grown in triplicates in SC-URA-LEU containing 2mM of AsV until exponential growth phase, and RNA was extracted, labeled, and hybridized to Affymetrix Yeast Genome S98 arrays.
2011-11-04 | E-GEOD-33427 | biostudies-arrayexpress