Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Wild type 3 hours exposure to 0.1 microM OGT2468

ABSTRACT: We did transcription profiling on the effect of O-glycosylation inhibitor OGT2468 in Saccharomyces cerevisiae using strains SEY6210 (wild type). Yeast cells exposed to OGT2468 in YPD growth medium show a significant inhibition of mating, filamentation and induction of cell wall compensatory mechanism. Three biological samples were analyzed for each condition, and a microarray experiment were carried out for each sample 1. absence of the drug (but the corresponding amount of DMSO 0.1%) 2. presence of 0.1 microMolar of OGT2468

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Javier Arroyo

PROVIDER: E-GEOD-12193 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:The capacity to sense and transduce temperature signals pervades all aspects of biology, and temperature exerts powerful control over the development and virulence of diverse pathogens. In the leading fungal pathogen of humans, Candida albicans, temperature has a profound impact on morphogenesis, a key virulence trait. Many cues that induce the transition from yeast to filamentous growth are contingent on a minimum temperature of 37ÂºC, while further elevatation to 39ÂºC serves as an independent inducing cue. The molecular chaperone Hsp90 is a key regulator of C. albicans temperature-dependent morphogenesis, as induction of filamentous growth requires relief from Hsp90-mediated repression of the morphogenetic program. Compromise of Hsp90 function genetically, pharmacologically, or by elevated temperature induces filamentation in a manner that depends on protein kinase A (PKA) signaling, but is independent of the terminal transcription factor, Efg1. Here, we determine that despite morphological and regulatory differences, inhibition of Hsp90 induces a transcriptional profile similar to that induced by other filamentation cues, and does so in a manner that is independent of Efg1. Further, we identify Hms1 as a transcriptional regulator required for morphogenesis induced by elevated temperature or compromise of Hsp90 function. Hms1 functions downstream of the cyclin Pcl, and the cyclin-dependent kinase Pho85, both of which are required for temperature-dependent filamentation. Upon Hsp90 inhibition, Hms1 binds to DNA elements involved in filamentous growth, including UME6 and RBT5, and regulates their expression, providing a mechanism through which Pho85, Pcl1, and Hms1 govern morphogenesis. Consistent with the importance of morphogenetic flexibility with virulence, deletion of C. albicans HMS1 attenuates virulence in a metazoan model of infection. Thus, we establish a new mechanism through which Hsp90 orchestrates C. albicans morphogenesis, and define novel regulatory circuitry governing a temperature-dependent developmental program, with broad implications for temperature sensing and virulence of microbial pathogens. Genome-wide occupancy experiments (Chip-CHIP) of FLAG-tagged Hms1p from cells grown in the presence or absence of geldanamycin (GldA). Co-precipitating genomic DNA was labelled and hybridized to whole-genome tiling arrays.

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Wild type 3 hours exposure to 0.1 microM OGT2468

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