Candida albicans
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ABSTRACT:
PROVIDER: PRJNA308800 | ENA |
REPOSITORIES: ENA
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Project description:Comparative analysis of genome wide binding profile of Ncb2 in azole sensitive (AS, Gu4) and azole resistant (AR, Gu5) clinical isolates of Candida albicans. The goal was to study the role of Ncb2 in acquisition of drug resistance by comparing the binding profiles of Ncb2 in both the isolates.
2017-08-01 | GSE76858 | GEO
Project description:Map ORC binding sites to identify replication origins in C. albicans by using polyclonal ORC antibodies (gift from Stephen Bell Lab). Due to the unsynchronized nature of Candida cells, log-phase cultures were taken to perfoem ChIP-chip experiments to find the genome-wide ORC binding sites.
2014-02-13 | GSE54923 | GEO
Project description:Map ORC binding sites to identify replication origins in C. albicans by using polyclonal ORC antibodies (gift from Stephen Bell Lab). Due to the unsynchronized nature of Candida cells, log-phase cultures were taken to perfoem ChIP-chip experiments to find the genome-wide ORC binding sites. ChIP-chip experiments from log-phase C. albicans culture. 7 different unsynchronized log-phase cultures as replicates.
2014-02-13 | E-GEOD-54923 | biostudies-arrayexpress
Project description:A major mechanism of azole resistance in Candida albicans is the over-expression of the genes encoding the ABC transporters Cdr1p and Cdr2p. Constitutive over-expression of these efflux pumps is due to mutations in the gene encoding Tac1p, resulting in hyperactivity of this zinc cluster transcription factor. In order to identify the transcriptional targets of Tac1p, we examined four matched sets of clinical isolates representing the development of CDR1- and CDR2-mediated azole resistance, using gene expression profiling analysis. We identified 31 genes that were consistently up-regulated with CDR1 and CDR2, including TAC1 itself, as well as 12 consistently down-regulated genes. When a resistant strain deleted for TAC1 was similarly examined, the expression of almost all of these genes was returned to levels similar to those in the matched azole-susceptible isolate. Keywords: gene expression profiling
2008-03-15 | GSE8727 | GEO
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 upc2Δ/Δ mutant than for its azole-susceptible parent, SC5314. Moreover, the upc2Δ/Δ mutant was unable to grow on a solid medium containing 10 µg/ml fluconazole and exhibited increased susceptibility and a clear zone of inhibition by Etest. Time-kill analysis showed higher fungistatic activity against the upc2Δ/Δ 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 µg/ml fluconazole and exhibited increased susceptibility and a clear zone of inhibition by Etest. Time-kill analysis showed increased fungistatic activity against the upc2Δ/Δ 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.
2014-05-24 | GSE57929 | GEO
Project description:A major mechanism of azole resistance in Candida albicans is the over-expression of the genes encoding the ABC transporters Cdr1p and Cdr2p. Constitutive over-expression of these efflux pumps is due to mutations in the gene encoding Tac1p, resulting in hyperactivity of this zinc cluster transcription factor. In order to identify the transcriptional targets of Tac1p, we examined four matched sets of clinical isolates representing the development of CDR1- and CDR2-mediated azole resistance, using gene expression profiling analysis. We identified 31 genes that were consistently up-regulated with CDR1 and CDR2, including TAC1 itself, as well as 12 consistently down-regulated genes. When a resistant strain deleted for TAC1 was similarly examined, the expression of almost all of these genes was returned to levels similar to those in the matched azole-susceptible isolate. Keywords: gene expression profiling Four clinical match isolates (azole susceptible and resistant) were grown as three independent replicates for each set to mid-log phase. A TAC1 knockout derived from resistant isolate 5674 was also grown as three independent replicates. Each resistant isolate was compared to its susceptible parent, and the TAC1 knockout was compared to the susceptible parent (5457) of the resistant isolate, 5674.
2010-05-25 | E-GEOD-8727 | biostudies-arrayexpress
Project description:UPC2 Is universally essential for Azole antifungal resistance in Candida albicans
| PRJNA248441 | ENA
Project description:ChIP-Chip of TAP-tagged Ppr1 Candida albicans strains
| PRJNA318644 | ENA
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.
2014-05-24 | E-GEOD-57929 | biostudies-arrayexpress