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RNA-sequencing analysis of fluconazole-treated wild-type and upc2A null cells [Fluconazole]

ABSTRACT: RNA-sequencing analysis of fluconazole-treated wild-type and upc2A null cells [Fluconazole]

PROVIDER: PRJNA756363 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15532700_1.fastq.gz	Fastqsanger.gz
	SRR15532700_2.fastq.gz	Fastqsanger.gz
	SRR15532689_1.fastq.gz	Fastqsanger.gz
	SRR15532689_2.fastq.gz	Fastqsanger.gz
	SRR15532690_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

RNA-sequencing analysis of fluconazole-treated wild-type and upc2A null cells [Fluconazole]

Project description:Purpose: Compare the fluconazole-induced transcriptome of isogenic wild-type and upc2A null cells. Methods: Prepare total RNA from wild-type and upc2A null cells grown under unstressed conditions or challenged with 50 microgram/ml fluconazole for 6 hours. Use standard RNA-seq to evaluate and compare the transcriptomic changes caused by fluconazole in the presence or absence of UPC2A. Results: These data established that over 100 genes were induced by fluconazole in a UPC2A-dependent manner. However, most fluconazole-induced genes (>500) did not require the presence of UPC2A. Fluconazole-induced genes included the expected genes involved in ergosterol biosynthesis but also large number of plasma membrane-localized transporters. Conclusions: These data suggest that Upc2A provided transcriptional co-regulation between membrane transporters and the lipid environment in which these proteins function. A significant portion of the fluconazole-induced transcriptome does not require the presence of Upc2A, suggesting the presence of other transcriptional circuits responsive to this pharmacologic block of ergosterol biosynthesis.

2021-09-23 | GSE182489 | GEO

RNA-seq Analysis of Wild-Type and G898D UPC2A Transcriptomes [G898D UPC2A transcriptome]

Project description:Purpose: Determine the number of genes that respond to the presence of a gain-of-function mutant form of the UPC2A transcription factor in Candida glabrata. Methods: Prepare total RNA from wild-type and gain-of-function G898D UPC2A cells. Use standard RNA-seq to evaluate and compare the transcriptomic changes caused by this allele of UPC2A. Results: Although a clear increase was seen in fluconazole resistance conferred by the G898D UPC2A allele, elevated transcription was only observed for 11 genes with 9 of these involved in ergosterol biosynthesis. Conclusions: The presence of the G898D UPC2A allele led to elevated constitutive transcription for genes involved in ergosterol biosynthesis.

2021-09-23 | GSE182490 | GEO

ChIP-seq analysis of transcription factor Upc2A binding across the Candida glabrata genome [Upc2A ChIP-seq]

Project description:To determine the genomic binding sites for the Candida glabrata transcription factor Upc2A, we utilized three different strains. One was the wild-type KKY2001 which contains a wild-type copy of UPC2A but lacks any HA tag. The other two are both derived from KKY2001 but contain a 3X HA tag immediately after the start codon of UPC2A. These strains are BVGC82 and BVGC84, respectively. Both contain a single copy of a loxP element located 252 bp downstream from the UPC2A stop codon. BVGC82 contains a wild-type copy of the UPC2A gene while BVGC84 contains a mutant form of UPC2A (G898D) that confers elevated resistance to fluconazole. ChIP was performed with anti-HA antibodies in all cases. Strains containing the wild-type UPC2A gene (no HA tag) are referred to as C1 and C2. Strains containing the 3X HA epitope tag at the N-terminus of the wild-type UPC2A gene are referred to as wt1 and wt2. These same strains challenged with fluconazole prior to ChIP are referred to as wtf1 and wtf2. The strain containing the G898D UPC2A allele are referred to as M1 and M2 (no fluconazole challenge) and MF1 and MF2 (with fluconazole challenge.

2021-09-23 | GSE182488 | GEO

Loss-of-function ROX1 mutations suppress the fluconazole susceptibility of upc2A∆ mutation in Candida glabrata, implicating additional positive regulators of ergosterol biosynthesis

Project description:Two of the major classes of antifungal drugs in clinical use target ergosterol biosynthesis. Despite its importance, our understanding of the transcriptional regulation of ergosterol biosynthesis genes in pathogenic fungi is essentially limited to the role of hypoxia and sterol-stress induced transcription factors such as Upc2 and Upc2A as well as homologs of Sterol Response Element Binding (SREB) factors. To identify additional regulators of ergosterol biosynthesis in Candida glabrata, an important human fungal pathogen with reduced susceptibility to ergosterol biosynthesis inhibitors relative to other Candida spp., we used a serial passaging strategy to isolate suppressors of the fluconazole hypersusceptibility of a upc2A∆ deletion mutant. This led to the identification of loss of function mutants in two genes: ROX1, the homolog of a hypoxia gene transcriptional suppressor in Saccharomyces cerevisiae, and CST6, a transcription factor that is involved in the regulation of carbon dioxide response in C. glabrata. Here, we describe a detailed analysis of the genetic interaction of ROX1 and UPC2A. In the presence of fluconazole, loss of Rox1 function restores ERG11 expression to the upc2A∆ mutant and inhibits the expression of ERG3 and ERG6, leading to increased levels or ergosterol and decreased levels of the toxic sterol, 14α methyl-ergosta-8,24(28)-dien-3β, 6α-diol, relative to upc2A∆. Our observations establish that Rox1 is a negative regulator of ERG gene biosynthesis and indicate that a least one additional positive transcriptional regulator of ERG gene biosynthesis must be present in C. glabrata.

2021-12-20 | GSE191145 | GEO

RNA-seq Analysis of Wild-Type and G898D UPC2A Transcriptomes [G898D UPC2A transcriptome]

Project description:RNA-seq Analysis of Wild-Type and G898D UPC2A Transcriptomes [G898D UPC2A transcriptome]

| PRJNA756364 | ENA

LFQP of lysates from wild-type, RAB18-, TBC1D20-, RAB3GAP1- and RAB3GAP2-null RPE1 cells

Project description:These data are from two wild-type RPE1 clones (WT11, WT20), a RAB18-null clone, a TBC1D20-null clone, a RAB3GAP1-null clone and a RAB3GAP2-null clone, each analysed in triplicate.

2024-01-26 | PXD016326 | Pride

LFQP of lysates from wild-type and TBC1D20-null HeLa cells

Project description:These data are from two wild-type HeLa clones (WT1, WT2) and two TBC1D20-null clones (5H2, 7H5), each analysed in triplicate.

2024-01-26 | PXD016233 | Pride

Expression Data from wild type and E2F4 null MEFs

Project description:We have used primary MEFs derived from wild type and E2F4 null mice growing asynchrounously in serum to generate a signature for E2F4 pathway activation. 10 wild type and 10 E2F4 null samples were each assayed using the Affymetrics Mouse Genome 430A 2.0 array. Keywords: Primary MEFs from wild type and E2F4 null mice

2008-07-11 | GSE11039 | GEO

Leishmania infantum: Alba20 null mutant Vs wild type

Project description:Transcriptome analysis of an LiAlba20 (LinJ.34.2410) null mutant strain versus Wild type. Experiments were run with promastigotes and axenic amastigotes independently. Null mutant was produced by homologous recombination, replacing both alleles with Hygromycin phosphotransferase and Puromycin.

2014-12-31 | GSE49825 | GEO

Expression data from ozone-treated wild-type and G-protein null mutant Arabidopsis lines

Project description:Ozone pollution decreases plant growth and yield worldwide. Some of the effects are genetically-mediated and are reported to involve G-protein signaling pathways. Effects of ozone on gene expression were examined in wild-type and G-protein null mutants to determine affected genes and to determine differential responses that may help define affected pathways. We used microarrays to examine changes in gene expression in response to ozone exposure and identified distinct classes of up- and down-regulated genes in wild-type and G-protein null mutant genotypes.

2011-12-24 | GSE34667 | GEO

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