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ATAC-seq identifies chromatin landscapes linked to the regulation of oxidative stress in the human fungal pathogen Candida albicans

ABSTRACT: ATAC-seq identifies chromatin landscapes linked to the regulation of oxidative stress in the human fungal pathogen Candida albicans

PROVIDER: PRJNA658373 | ENA |

REPOSITORIES: ENA

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ATAC-seq identifies chromatin landscapes linked to the regulation of oxidative stress in the human fungal pathogen Candida albicans

Project description:ATAC-seq analysis of Candida albicans SC5314 treated or not treated with hydrogen peroxide to assess the accessible chromatin landscape upon oxidative stress in comparison to normal growth in YPD at 30 °C.

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ATAC-Seq Identifies Chromatin Landscapes Linked to the Regulation of Oxidative Stress in the Human Fungal Pathogen Candida albicans.

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The spliceosome impacts morphogenesis in the human fungal pathogen Candida albicans.

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Transcriptional control of hypoxic hyphal growth in the fungal pathogen Candida albicans

Project description:So far, there is no known regulatory circuits that mediate filamentation of the pathogenic yeast Candida albicans exclusively in response to hypoxia. In this study, we performed a quantitative analysis of gene deletion mutants from different collections of protein kinases and transcriptional regulators to identify specific regulator of the hypoxic filamentation. Our work uncovered two transcription factors, Ahr1 and Tye7, that act as prominent regulators of C. albicans filamentation specifically under hypoxia. In summary, we used genome-wide transcriptional profiling and promoter occupancy to characterize both Ahr1 and Tye7 regulons associated with the hypoxic filamentation in C. albicans.

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Project description:Inside the human host, the pathogenic yeast Candida albicans colonizes predominantly oxygen-poor niches such as the gastrointestinal and vaginal tracts, but also oxygen-rich environments such as cutaneous epithelial cells and oral mucosa. This suppleness requires an effective mechanism to reprogram reversibly the primary metabolism in response to oxygen variation. Here, we have uncovered that Snf5, a subunit of SWI/SNF chromatin remodeling complex, is a major transcriptional regulator that links oxygen status to the metabolic capacity of C. albicans. Snf5 and other subunits of SWI/SNF complex were required to activate genes of carbon utilization and other carbohydrates related process specifically under hypoxia. snf5 mutant exhibited an altered metabolome reflecting that SWI/SNF plays an essential role in maintaining metabolic homeostasis and carbon flux in C. albicans under hypoxia. Snf5 was necessary to activate the transcriptional program linked to both commensal and invasive growth. Accordingly, snf5 was unable to maintain its growth in the stomach, the cecum and the colon of mice. snf5 was also avirulent as it was unable to invade Galleria larvae or to cause damage to human enterocytes and murine macrophages. Among candidates of signaling pathways in which Snf5 might operate, phenotypic analysis revealed that mutants of Ras1-cAMP-PKA pathway, as well as mutants of Yak1 and Yck2 kinases exhibited a similar carbon flexibility phenotype as did snf5 under hypoxia. Genetic interaction analysis indicated that the adenylate cyclase Cyr1, a key component of the Ras1-cAMP pathway genetically with Snf5. Our study yielded new insight into the oxygen-sensitive regulatory circuit that control metabolic flexibility, stress, commensalism and virulence in C. albicans.

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Project description: Not available

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