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ABSTRACT: Candida auris adhesive variants RNA seq

PROVIDER: PRJNA904261 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22376027_1.fastq.gz	Fastqsanger.gz
	SRR22376027_2.fastq.gz	Fastqsanger.gz
	SRR22376028_1.fastq.gz	Fastqsanger.gz
	SRR22376028_2.fastq.gz	Fastqsanger.gz
	SRR22376029_1.fastq.gz	Fastqsanger.gz

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Project description:Candida auris adhesive transposon mutants WGS

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High-throughput RNA Sequencing of BMDM of Mus musculus stimulated by C. auris or C. albicans

Project description:Candida auris has been globally recognized as a multidrug-resistant human fungal pathogen that contributes for the worldwide occurrence of nosocomial outbreaks. It has been reported that C. auris was able to avoid neutrophil attack, suggestive of an impaired innate immune response. Whether C. auris evades the innate immune recognition of BMDM (bone marrow derived macrophage) remains poorly understood, and as for well-known Candida species -C. albicans, it can trigger immune response. To determine whether occurs difference between immune response stimulated by C. auris or C. albicans, we performed mRNA-seq of BMDM stimulated by C. auris or C. albicans.

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Project description:Transcriptomic analysis of different Candida auris clinical isolates with distinct antifungal susceptibility profiles.

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Project description:Candida auris clinical isolate FY279 was exposed to tebuconazole (32μg/ml). Randomly14 adaptors were chosen. 10 adaptors obtained resistance to tebuconazole. These resistant adaptors were sequenced.

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Project description:Filamentous cell growth is a vital property of fungal pathogens. The mechanisms of filamentation in the emerging multidrug-resistant fungal pathogen Candida auris are poorly understood. Here, we show that exposure of C. auris to glycerol triggers a rod-like filamentation-competent (RL-FC) phenotype, which forms elongated filamentous cells after a prolonged culture period. Whole-genome sequencing analysis reveals that all RL-FC isolates harbor a mutation in the C2H2 zinc finger transcription factor-encoding gene GFC1 (Gfc1 variants). Deletion of GFC1 leads to an RL-FC phenotype similar to that observed in Gfc1 variants. We further demonstrate that GFC1 mutation causes enhanced fatty acid β-oxidation metabolism and thereby promotes RL-FC/filamentous growth. This regulation is achieved through a Multiple Carbon source Utilizer (Mcu1)-dependent mechanism. Interestingly, both the evolved RL-FC isolates and the gfc1Δ mutant exhibit an enhanced ability to colonize the skin. Our results reveal that glycerol-mediated GFC1 mutations are beneficial during C. auris skin colonization and infection.

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Project description:Approximately 1 million cells of Candida auris isolate FY279 were spread on YPD plate supplemented with 8ug/ml tunicamycin. Randomly 21 adaptors were chosen. These adaptors were sequenced.

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Potent synergistic interactions between lopinavir and azole antifungal drugs against emerging multidrug-resistant Candida auris

Project description:The limited number of antifungals and the emergence of multidrug-resistant Candida auris pose a significant challenge to human medicine. Here, we utilized combinatorial drug therapy as an approach to augment the activity of current azole antifungals against C. auris. We evaluated the fluconazole chemosensitization activity of 1547 FDA-approved drugs and clinical molecules against an azole-resistant strain of C. auris. This led to the discovery that lopinavir, an antiviral drug, is a potent agent capable of sensitizing C. auris to the effect of azole antifungals. At a therapeutically achievable concentration (4-8 µg/ml), lopinavir exhibited potent synergistic interactions with azole drugs, particularly with itraconazole, against C. auris (ΣFICI ranged from 0.05-0.50). The lopinavir/itraconazole combination enhanced the survival rate of C. auris-infected Caenorhabditis elegans by 90% and reduced the fungal burden in infected nematodes by 88.5% (p < 0.05). Moreover, lopinavir enhanced the antifungal activity of itraconazole against other medically important Candida species including C. albicans, C. tropicalis, C. glabrata, C. tropicalis, and C. parapsilosis. Comparative transcriptomic profiling revealed that lopinavir interferes with glucose permeation and ATP synthesis. This compromises the function of the efflux pumps presents in C. auris enhancing sensitivity to azole antifungals, as demonstrated by Nile red efflux assays. This study presents lopinavir as a novel, potent and broad-spectrum azole chemosensitizing agent that warrants further investigation against recalcitrant Candida infections.

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