Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA119087 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Wild type (BY4741) Saccharomyces cerevisiae strains and their isogenic slt2 deficient counterparts, were treated for 2 hours with sodium arsenate 100 micromolar. Control (untreated) cells were also collected. Total RNA was extracted and analyzed by microarray hybridization. The data obtained from these experiments allows to determine those genes that are regulated by Slt2 activity after arsenate treatment.
2010-07-25 | GSE17364 | GEO
Project description:Wild type (BY4741) Saccharomyces cerevisiae strains and their isogenic slt2 deficient counterparts, were treated for 2 hours with sodium arsenate 100 micromolar. Control (untreated) cells were also collected. Total RNA was extracted and analyzed by microarray hybridization. The data obtained from these experiments allows to determine those genes that are regulated by Slt2 activity after arsenate treatment. The experiments was designed as follows: Four types of samples were used: untreated wild type cells, treated wild type cells, untreated slt2- cells and treated slt2- cells. 3 independent replicates were performed for each experiment.
2010-07-25 | E-GEOD-17364 | biostudies-arrayexpress
Project description:Expression data from yeast exposed to Caspofungin (wild type strain and rlm1, slt2, msn2/4 and bcy1 mutants) and Aminocandin (wild type strain)
| PRJNA318793 | ENA
Project description:Heme Deficient vs Wild Type in Low Iron
| PRJNA93417 | ENA
Project description:RNA-sequencing of Aire-ILC3 cells from wild-type and Aire-deficient mice
2019-01-16 | E-MTAB-7088 | ExpressionAtlas
Project description:Transcription profiling by array of bone marrow cells from wild type, Fancc-deficient, Fancg-deficient, and doubly deficient (Fancc/Fancg) mice
2014-07-03 | E-GEOD-22094 | ExpressionAtlas
Project description:Genome-wide Response of Saccharomyces cerevisiae upon Arsenate Exposure
| PRJNA148865 | ENA
Project description:Arsenic is known as a human carcinogen that easily be exposed by the living organisms through environment and food consumption. The arsenic is transport into the cells via phosphate transporters due to its structural similarity with phosphate in both prokaryotes and eukaryotes. We here evaluated and analyzed the toxicogenomic impacts of arsenate and the role of different phosphate concentrations on arsenic toxicity. Our results showed that arsenic uncoupled phosphate levels which eventually affected the growth rate of yeast cells. Analysis of arsenate levels in the medium over 4 to 10 h of its exposure clearly showed that arsenate was easily taken up by the cells in phosphate limited condition.
2009-12-31 | GSE14991 | GEO
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.
2011-11-04 | GSE33427 | GEO