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Candida albicans

ABSTRACT: Candida albicans clinical isolates exposed to fluconazole

PROVIDER: PRJNA638239 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11962746.fastq.gz	Fastqsanger.gz
	SRR11962747.fastq.gz	Fastqsanger.gz
	SRR11962748.fastq.gz	Fastqsanger.gz
	SRR11962749.fastq.gz	Fastqsanger.gz
	SRR11962750.fastq.gz	Fastqsanger.gz

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The early transcriptional and post-transcriptional responses to fluconazole in sensitive and resistant Candida albicans (RNA-Seq)

Project description:Candida albicans is a leading cause of fungal infections in immunocompromised patients. Management of candidemia relies on a few antifungal agents, with fluconazole being first line therapy. The emergence of fluconazole-resistant strains highlights the pressing need to improve our molecular understanding of the drug response mechanisms. By sequencing the 5’P mRNA degradation intermediates, we show that co-translational mRNA decay is common in C. albicans and characterize how in vivo 5´-3´ exonuclease degradation trails the last translating ribosome. Thus, the study of the 5'P mRNA degradome (5PSeq) offers a simple and affordable way to measure ribosome dynamics and identify codon specific ribosome stalls in response to drugs and amino acid deprivation. Building upon this, we combine RNA-Seq and 5PSeq to study the early response of sensitive and resistant C. albicans isolates to fluconazole. Our results highlight that transcriptional responses, rather than changes in ribosome dynamics, are the main driver of Candida resistance to fluconazole.

2024-10-06 | GSE267941 | GEO

The early transcriptional and post-transcriptional responses to fluconazole in sensitive and resistant Candida albicans (5P-Seq)

2024-10-06 | GSE267940 | GEO

Up-regulation of ERG11 is prevalent among azole-resistant clinical isolates of Candida albicans and is only partially explained by gain-of-function mutations in UPC2

Project description:In Candida albicans, Upc2 is a zinc-cluster transcription factor that targets genes including those of the ergosterol biosynthesis pathway. To date there have been three documented UPC2 gain-of-function (GOF) mutations recovered from fluconazole-resistant clinical isolates that contribute to an increase in ERG11 expression and decreased fluconazole susceptibility. In a group of 62 fluconazole-resistant isolates, we found that 47 of these overexpressed ERG11 by at least two-fold over that of an average expression of 3 unrelated fluconazole susceptible strains. Of those 47 isolates, 29 contained a mutation in UPC2, whereas the remaining 18 isolates did not. Of the isolates containing mutations in UPC2, we recovered eight distinct mutations resulting in single putative amino acid substitutions: G648D, G648S, A643T, A643V, Y642F, G304R, A646V and W478C. Seven of these resulted in increased ERG11 expression, increased cellular ergosterol, and decreased susceptibility to fluconazole as compared to the wild-type strain. Genome-wide transcriptional analysis was performed for the four strongest Upc2 amino acid substitutions (A643V, G648D, G648S and Y642F). Genes commonly upregulated in all four mutations included those involved in ergosterol biosynthesis, in oxidoreductase activity, the major facilitator efflux pump encoded by the MDR1 gene, and the uncharacterized ATP binding cassette transporter CDR11. These findings demonstrate that gain-of-function mutations in UPC2 are more prevalent than previously thought among clinical isolates, make a significant contribution to azole antifungal resistance, but do not account for ERG11 overexpression in all such isolates of C. albicans.

2013-01-31 | GSE39201 | GEO

Transcriptome analysis of Candida albicans exposed to sub-inhibitory amount of fluconazole

Project description:Candida albicans lab strain SC5314 was exposed to 0.5ug/ml fluconazole for 3h. Transcriptome was compared to no drug control.

2022-07-08 | E-MTAB-11881 | biostudies-arrayexpress

Whole genome sequencing of fluconazle resistant and tolerant adaptors in Candida albicans

Project description:Candida albicans lab strain SC5314 was daily passaged in YPD broth supplemented with fluconazole. Some fluconazole-resistant and some fluconazole-tolerant adaptors were sequenced.

2022-10-10 | E-MTAB-12189 | biostudies-arrayexpress

CGH analysis of Candida albicans strains

Project description:Aneuploidy and the evolution of aneuploid karyotypes of Candida albicans strains was identified using aCGH. Whole chromosome and segmental aneuploidies, (specifically on the left arm of chromosome 5 - shown to be due to isochromosome formation) are associated with the appearance of resistance to the antifungal drug fluconazole. Keywords: Comparative Genomic Hybridization

2006-06-30 | GSE4995 | GEO

Transcription profiling of Candida albicans clinical isolates

Project description:Comparison of 20 clinical isolates of Candida albicans grown under identical growth conditions (biofilm growth conditions in RPMI 1640/10% serum)

2009-02-11 | E-MEXP-1933 | biostudies-arrayexpress

Mistranslation accelerates the adaptation of Candida albicans to Fluconazole

Project description:The leucine CUG codon was reassigned to serine in the fungal pathogen Candida albicans. To clarify the biological role of this tuneable codon ambiguity on drug resistance, we evolved C. albicans strains that were engineered to mistranslate the CUG codon at constitutively elevated levels, in the presence and absence of the antifungal drug fluconazole. Elevated levels of mistranslation resulted in the rapid acquisition of resistance to fluconazole.

2016-10-27 | E-SYBR-13 | biostudies-arrayexpress

The proteomics of Candida albicans

Project description:The proteomics of different isolates of Candida albicans

2022-03-07 | PXD032114 |

Lactate- and hypoxia-induced beta-glucan masking in responding and non-responding Candida albicans clinical isolates

Project description:RNA sequencing was performed on Candida albicans clinical isolates that display normal (isolates: 3560, 3605, 3609, 4108, 4259) or aberrant (isolates: 3534, 3544, 3621, 3636, 4036) beta-glucan masking in response to lactate and hypoxia. Each clinical isolate was grown to exponential phase in GYNB under normoxic conditions and then exposed for 5 h to: (a) 1% lactate; (b) 0% lactate control; (c) hypoxia; or (d) normoxic control. Three independent experiments were performed for each clinical isolate.

2023-09-05 | E-MTAB-10986 | biostudies-arrayexpress

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