Transcriptional profile of pmt1 pmt4 mutants
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
PROVIDER: GSE12182 | GEO | 2010/09/30
SECONDARY ACCESSION(S): PRJNA114655
REPOSITORIES: GEO
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Project description:We did transcription profiling on the effect of pmt1 pmt2 deletion. These genes are involved in the O-glycosylation process. These mutants cells show inhibition of mating, filamentation and induction of cell wall compensatory mechanism.
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Project description:We did transcription profiling on the effect of pmt1 pmt4 deletion, genes involved in the O-glycosylation process. These mutants cells show inhibition of mating, filamentation and induction of cell wall compensatory mechanism. Two biological samples were analyzed for each condition, and a microarray experiment were carried out for each sample 1. wild type cells SEY6210 2. pmt1 pmt2 cells from SEY6210 background
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Project description:We did transcription profiling on the effect of pmt1 pmt2 deletion. These genes are involved in the O-glycosylation process. These mutants cells show inhibition of mating, filamentation and induction of cell wall compensatory mechanism. Two biological samples were analyzed for each condition, and a microarray experiment were carried out for each sample 1. wild type cells SEY6210 2. pmt1 pmt2 cells from SEY6210 background
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Project description: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.
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Project description: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.
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Project description: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
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Project description: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 1%) 2. presence of 1 microMolar of OGT2468
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Project description:Candida albicans is an opportunistic fungal pathogen capable of causing superficial and systemic infections in humans. The ability of C. albicans to switch between various morphological forms depending on its host environment is thought to contribute to its virulence. Filamentous growth states are associated with tissue invasion, biofilm formation, evasion of innate host defences and mating. Although the mechanisms of activation of filamentous growth pathways are well understood, less is known about which factors control the negative regulation of filamentation. In this study, we have identified a previously uncharacterized Orf that shares sequence similarity with Saccharomyces cerevisiae Dig1p and Dig2p. Deletion of the gene encoding this Orf triggers invasive growth in C. albicans and so we have retained the yeast designation of Dig1 (for Down-regulation of Invasive Growth). Mutants lacking CaDIG1 form cultures of hyperpolarized cells, form robust biofilms, are highly invasive in vitro but not in vivo and are constitutively activated for the pheromone response. Deletion of key transcription factors that act downstream of Dig1p provide evidence to suggest that CaDig1 regulates filamentation and mating through multiple signalling pathways.
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Project description:DNA sequencing of Paramecium tetraurelia mating type mutants
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Project description:Candida albicans is an opportunistic fungal pathogen capable of causing superficial and systemic infections in humans. The ability of C. albicans to switch between various morphological forms depending on its host environment is thought to contribute to its virulence. Filamentous growth states are associated with tissue invasion, biofilm formation, evasion of innate host defences and mating. Although the mechanisms of activation of filamentous growth pathways are well understood, less is known about which factors control the negative regulation of filamentation. In this study, we have identified a previously uncharacterized Orf that shares sequence similarity with Saccharomyces cerevisiae Dig1p and Dig2p. Deletion of the gene encoding this Orf triggers invasive growth in C. albicans and so we have retained the yeast designation of Dig1 (for Down-regulation of Invasive Growth). Mutants lacking CaDIG1 form cultures of hyperpolarized cells, form robust biofilms, are highly invasive in vitro but not in vivo and are constitutively activated for the pheromone response. Deletion of key transcription factors that act downstream of Dig1p provide evidence to suggest that CaDig1 regulates filamentation and mating through multiple signalling pathways. Transcriptional analysis of the C. albicans dig1Δ/dig1Δ homozygous mutant versus the wild type (SN148) in the MTLa/alpha background. Four biological replicates of the mutant and the wild type were included in the analysis. Samples were grown at 30 °C in YPD medium plus uridine
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