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ABSTRACT: Cryptococcus deneoformans sRNA sequencing

PROVIDER: PRJNA726800 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14385249.fastq.gz	Fastqsanger.gz
	SRR14385250.fastq.gz	Fastqsanger.gz
	SRR14385251.fastq.gz	Fastqsanger.gz
	SRR14399787.fastq.gz	Fastqsanger.gz
	SRR14399788.fastq.gz	Fastqsanger.gz

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A velvet transcription factor specifically activates mating through a novel surface protein in the human fungal pathogen Cryptococcus deneoformans

Project description:Sexual reproduction facilitates infection by the production of both a lineage advantage and infectious sexual spores in the ubiquitous human fungal pathogen Cryptococcus deneoformans. However, the regulatory determinants specific for initiating mating remain poorly understood. Here, we identified a velvet family regulator, Cva1, that strongly promotes sexual reproduction in C. deneoformans. This regulation was determined to be specific, based on a comprehensive phenotypic analysis of cva1 under 25 distinct in vitro and in vivo growth conditions. We further revealed that Cva1 plays a critical role in the initiation of early mating events, especially sexual cell-cell fusion, but is not important for the late sexual development stages or meiosis. Thus, Cva1 specifically contributes to mating activation. Importantly, a novel mating-responsive surface protein, Cfs1, serves as the key target of Cva1 during mating, since its absence nearly blocks cell-cell fusion in C. deneoformans and its sister species C. neoformans. Together, our findings provide insight into how C. deneoformans ensures regulatory specificity of mating.

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Project description:Sexual reproduction facilitates infections and adaptations in Cryptococcus pathogens that cause fatal meningoencephalitis and have two distinct sexual cycles (bisexual and unisexual). Here, by constructing a gene-deletion strains library for transcription factor (TF) genes in Cryptococcus deneoformans, we explore spatiotemporal TF networks in sequential stages of mating community development and identified key regulators that determine processes specific to different reproductive modes. We show that the TFs crucial for bisex-specific syngamy coordinately induce the expression of a specific group of genes centered on the ancient mating determinants, which includes FMP1, a previously unidentified component of the conserved fungal mating pathway. Furthermore, we identify that a recently evolved regulatory cascade mediates the pre-meiotic autodiploidization process that defines Cryptococcus unisex, supporting that unisex is a recent evolutionary innovation. Our findings indicate that genetic circuits with different evolutionary ages govern the hallmark events distinguishing unisex and bisex, enabling reproductive flexibility that benefits Cryptococcus pathogenicity.

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Amoeba Predation of Cryptococcus: A Quantitative and Population Genomic Evaluation of the Accidental Pathogen Hypothesis

Project description:The “Amoeboid Predator-Fungal Animal Virulence Hypothesis” posits that interactions with environmental phagocytes shape the evolution of virulence traits in fungal pathogens. In this hypothesis, selection to avoid predation by amoeba inadvertently selects for traits that contribute to fungal escape from phagocytic immune cells. Here, we investigate this hypothesis in the human fungalpathogens Cryptococcus neoformans and Cryptococcus deneoformans. Applying quantitative trait locus (QTL) mapping and comparative genomics, we discovered a cross-species QTL region that is responsible for variation in resistance to amoeba predation. In C. neoformans, this same QTL was found to have pleiotropic effects on melanization, an established virulence factor. Through fine mapping and population genomic comparisons, we identified the gene encoding the transcription factor BZP4 that underlies this pleiotropic QTL and we show that decreased expression of this gene reduces melanization and increases susceptibility to amoeba predation. Despite the joint effects of BZP4 on amoeba resistance and melanin production, we find no relationship between BZP4 genotype and escape from macrophages or virulence in murine models of disease. Our findings provide new perspectives on how microbial ecology shapes the genetic architecture of fungal virulence, and suggests the need for more nuanced models for the evolution of pathogenesis that account for the complexities of both microbe-microbe and microbe-host interactions.

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