Unknown,Transcriptomics,Genomics,Proteomics

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Transcriptional profile of Candida parapsilosis CLIB214 versus UPC2 delete, both at 1% oxygen (hypoxia)

ABSTRACT: Whole genome microarray were used to generate the transcriptional profile of C. parapsilosis UPC2 delete in hypoxia. RNA was isolated from CLIB214 or upc2 delete grown in YPD medium in hypoxia at 30 degree Celsius for 2 h, and labeled with Cy3 or Cy5. Four independent biological replicates were compared. 2 dye swaps were perfomed so that 2 out of 4 samples isolated from CLIB214 in hypoxic culture were labeled with Cy3, and 2 were labeled with Cy5

ORGANISM(S): Candida parapsilosis

SUBMITTER: Geraldine Butler

PROVIDER: E-GEOD-32713 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:In Candida albicans, the transcription factor Upc2 is central to the regulation of ergosterol biosynthesis. UPC2-activating mutations contribute to azole resistance, whereas disruption increases azole susceptibility. In the present study, we investigated the relationship of UPC2 to fluconazole susceptibility, particularly in azole-resistant strains. In addition to the reduced fluconazole MIC previously observed with UPC2 disruption, we observed a lower minimum fungicidal concentration (MFC) for a upc2M-NM-^T/M-NM-^T mutant than for its azole-susceptible parent, SC5314. Moreover, the upc2M-NM-^T/M-NM-^T mutant was unable to grow on a solid medium containing 10 M-BM-5g/ml fluconazole and exhibited increased susceptibility and a clear zone of inhibition by Etest. Time-kill analysis showed higher fungistatic activity against the upc2M-NM-^T/M-NM-^T mutant than against SC5314. UPC2 disruption in strains carrying specific resistance mutations also resulted in reduced MICs and MFCs. UPC2 disruption in a highly azole resistant clinical isolate containing multiple resistance mechanisms likewise resulted in a reduced MIC and MFC. This mutant was unable to grow on a solid medium containing 10 M-BM-5g/ml fluconazole and exhibited increased susceptibility and a clear zone of inhibition by Etest. Time-kill analysis showed increased fungistatic activity against the upc2M-NM-^T/M-NM-^T mutant in the resistant background. Microarray analysis showed attenuated induction by fluconazole of genes involved in sterol biosynthesis, iron transport, or iron homeostasis in the absence of UPC2. Taken together, these data demonstrate that the UPC2 transcriptional network is universally essential for azole resistance in C. albicans and represents an attractive target for enhancing azole antifungal activity. We examined the genome-wide gene expression profiles of the wild-type parent strain SC5314 and its upc2M-NM-^T/M-NM-^T derivative in response to fluconazole in order to identify genes whose expression in response to fluconazole is influenced by Upc2.

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Transcriptional profile of Candida parapsilosis CLIB214 versus UPC2 delete, both at 1% oxygen (hypoxia)

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