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Endocytosis mediated by END3 is required for in vivo virulence of the opportunistic fungal pathogen Candida albicans

microbiology
mycology

Abstract

Endocytic trafficking is a fundamental cellular process that is crucial for Candida albicans secretion, filamentation, and virulence-related processes. We have previously demonstrated that loss of the key endocytosis-related gene END3 disrupts clathrin-mediated endocytosis, leading to impairments in actin patch formation, filamentation, biofilm formation, cell wall integrity, and extracellular protease secretion. The end3 null mutant also exhibits altered antifungal susceptibility and reduced host cell damage in an in vitro keratinocyte infection model. To ascertain whether endocytosis is required for virulence in vivo, we assessed virulence of the C. albicans end3 null mutant in a murine model of disseminated candidiasis. After infection via the tail vein and analysis of host survival over 28 days, the end3 null mutant was markedly hypovirulent compared to corresponding control strains. These results indicate that endocytosis mediated by END3 in C. albicans contributes to pathogenesis in vivo.
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