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The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus [ChIP-seq]

ABSTRACT: The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus [ChIP-seq]

PROVIDER: PRJNA533304 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8923330_1.fastq.gz	Fastqsanger.gz
	SRR8923330_2.fastq.gz	Fastqsanger.gz
	SRR8923331_1.fastq.gz	Fastqsanger.gz
	SRR8923331_2.fastq.gz	Fastqsanger.gz
	SRR8923332_1.fastq.gz	Fastqsanger.gz

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The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus [ChIP-seq]

Project description:The Negative cofactor 2 (NCT) complex is an evolutionally conserved heterodimeric transcription factor. In Aspergillus fumigatus, the NCT complex consists of two subunits NctA and NctB. Through a genome-wide screening of a transcription factor null mutant strains, we found that loss of the NCT complex leads to a multi-drug resistance phenotype including the azoles (itraconazole, voriconazole and posaconazole) as well as the salvage therapeutic amphotericin B, and terbinafine. To obtain further insight into the molecular mechanisms driving the azole-resistance in the NCT complex null mutants, we analyzed genome-wide binding profiles of NctA using chromatin-immunoprecipitation sequencing (ChIP-seq). Our ChIP-seq analysis revealed that NCT complex binds the promoters of several ergosterol biosynthetic genes, their transcriptional regulators, and the azole efflux pump cdr1B. Taken together, these results suggest that the NCT complex plays a role as a master regulator of drug resistance in A. fumigatus.

2019-12-31 | GSE129967 | GEO

The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus [RNA-seq]

Project description:The Negative cofactor 2 (NCT) complex is an evolutionally conserved heterodimeric transcription factor. In Aspergillus fumigatus, the NCT complex consists of two subunits NctA and NctB. Through a genome-wide screening of a transcription factor null mutant strains, we found that loss of the NCT complex leads to a multi-drug resistance phenotype including the azoles (itraconazole, voriconazole and posaconazole) as well as the salvage therapeutic amphotericin B, and terbinafine. To obtain further insight into the molecular mechanisms driving the azole-resistance in the NCT complex null mutants, we analyzed genome-wide gene expression profiles of the nctA and the nctB null mutants using RNA-seq. Our expression profiling revealed that disruption of the genes lead to upregulation of several ergosterol biosynthetic genes, their transcriptional activators, and the azole efflux pump cdr1B. Taken together, these results suggest that the NCT complex plays a role as a master regulator of drug resistance in A. fumigatus.

2019-12-31 | GSE133464 | GEO

The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus

Project description:The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus

| PRJNA551610 | ENA

The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus [RNA-seq]

Project description:The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus [RNA-seq]

| PRJNA551498 | ENA

The Negative Cofactor 2 complex is a master regulator of drug resistance in Aspergillus fumigatus

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-12-31 | GSE133491 | GEO

The negative cofactor 2 complex is a key regulator of drug resistance in Aspergillus fumigatus.

Project description:The frequency of antifungal resistance, particularly to the azole class of ergosterol biosynthetic inhibitors, is a growing global health problem. Survival rates for those infected with resistant isolates are exceptionally low. Beyond modification of the drug target, our understanding of the molecular basis of azole resistance in the fungal pathogen Aspergillus fumigatus is limited. We reasoned that clinically relevant antifungal resistance could derive from transcriptional rewiring, promoting drug resistance without concomitant reductions in pathogenicity. Here we report a genome-wide annotation of transcriptional regulators in A. fumigatus and construction of a library of 484 transcription factor null mutants. We identify 12 regulators that have a demonstrable role in itraconazole susceptibility and show that loss of the negative cofactor 2 complex leads to resistance, not only to the azoles but also the salvage therapeutics amphotericin B and terbinafine without significantly affecting pathogenicity.

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TAp73 is a master regulator of airway multiciliogenesis

Project description:TAp73 is a master regulator of airway multiciliogenesis

| PRJNA305139 | ENA

Transcriptional regulation of the thymus master regulator Foxn1

Project description:Transcriptional regulation of the thymus master regulator Foxn1

| PRJNA793576 | ENA

Monitoring the mating-type-driven transcriptomes of Aspergillus fumigatus

Project description:Sexual identity of the human pathogenic mold Aspergillus fumigatus is determined by the mating-type idiomorphs MAT1-1 and MAT1-2 residing at the MAT locus. Given that the MAT1 gene products are DNA binding master regulators that govern fruiting body formation, the MAT1-driven transcriptomes of A. fumigatus were monitored by conditional overexpression of either MAT1 gene followed by RNA-seq analyses.

2018-10-09 | GSE113404 | GEO

HMGA1: A master regulator of tumor progression in triple-negative breast cancer cells

Project description:Emerging evidence suggests that tumor cells metastasize by co-opting stem cell transcriptional networks, although the molecular underpinnings of this process are poorly understood. Here, we show for the first time that the high mobility group A1 (HMGA1) gene drives metastatic progression in triple negative breast cancer cells (MDA-MB-231) by reprogramming cancer cells to a stem-like state. We discovered an HMGA1 signature in triple negative breast cancer cells that is highly enriched in embryonic stem cells. Together, these findings indicate that HMGA1 is a master regulator of tumor progression in breast cancer by reprogramming cancer cells through stem cell transcriptional networks. Future studies are needed to determine how to target HMGA1 in therapy. HMGA1 was knocked-down in MDA-MB-231 cells using siRNA as we previously described (Tesfaye A 2007). RNA from three independent knockdown experiements along with 3 control populations were collected by Rneasy miniprep (Qiagen) and analyzed by Affymetrix Human Exon 1.0 ST platform.

2015-02-18 | E-GEOD-45483 | biostudies-arrayexpress

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