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Interplay of phosphate transport and tor through Pho84during Candida albicans gastrointestinal commensalism

Interplay of phosphate transport and TOR through Pho84during...

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多彩菌物美丽中国——中国菌物学会2019年学术年会

作者： Yuanyuan Wang Lin Liu Wanjun Qi Maikel Acosta-Zaldívar.angelique Besold Kicki Ryman Hiroto Kambara Hongbo R.Luo Per Olof Ljungdahl Valeria C.Culotta Jose L.Lopez-Ribot Hui Wang Julia R.K?hler Changbin Chen Ning-Ning Liu Unit of Pathogenic Fungal Infection ＆ Host Immunity CAS Key Laboratory of Molecular Virology ＆Immunology Institut Pasteur of Shanghai Chinese Academy of Sciences School of Public Health Shanghai Jiao Tong University School of Medicine Division of Infectious Diseases Boston Children’s Hospital/Harvard Medical School Department of Biochemistry and Molecular Biology The Johns Hopkins University Bloomberg School of Public Health Department of Molecular Biosciences The Wenner-Gren Institute Stockholm University Department of Pathology Joint Program in Transfusion Medicine Boston Children’s Hospital/Harvard Medical School Department of Biology University of Texas at San Antonio

Candida albicans is a commensal fungal pathogen which colonized in the human gut by adapting to various nutrients in the microenvironment. Pho84, a phosphate transceptor, is known to be crucial for maintenance of both phosphate homeostasis and torC1 activity which is required for Candida albicans virulence. In a mouse model of commensalism, loss of pho84 decreased C. albicans commensalism in both single and competitive mix infection. Overexpression of GTR1 or GTR1-GTP which hyperactivate torC1 activity moderately rescued the gastrointestinal colonization defect. Furthermore, the colonization defect of the pho84 null mutant was partially complemented through feeding mice with high Pi diet. Interestingly, during gut commensalism high Pi significantly restores GI tract colonization to the WT level when combined with overexpression of GTR1 or GTR1-GTP in the pho84 null mutant. Finally, in vivo studies demonstrate that the downstream commensalism-related genes expression were upregulated with either high Pi or torC1 *** vitro Caco2 cell infection model confirms that Pho84 promotes C. albicans adhesion to the intestinal epithelial cells through both Pi transport and tor. Thus, our findings unravel a mechanism by which Pho84 promotes gut commensalism through the interplay between phosphate transport and tor.activation.

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