Role of Hog1-mediated stress tolerance in biofilm formation by the pathogenic fungus Trichosporon asahii

Abstract

Trichosporon asahii, a dimorphic fungus, causes bloodstream infections in immunocompromised patients with neutropenia. Biofilms are formed on the surfaces of medical devices such as catheters as T. asahii transitions morphologically from yeast to hyphae in the host environment. Oxidative stress tolerance and morphological changes of T. asahii are regulated by Hog1, a mitogen-activated protein kinase. The role of Hog1 in the biofilm formation by T. asahii, however, has remained unknown. In the present study, we demonstrated that a hog1 gene-deficient T. asahii mutant formed excess biofilm under a rich medium in vitro, but did not form biofilm in an in vivo evaluation system using silkworms. The hog1 gene-deficient T. asahii mutant formed a greater amount of biofilm than the parent strain in vitro. Under an oxidative stress condition in vitro, however, lower amounts of biofilm were formed by the hog1 gene-deficient T. asahii mutant than by the parent strain. In an in vivo evaluation system using silkworms, lower amounts of biofilm were formed by the hog1 gene-deficient T. asahii mutant than by the parent strain. Our findings suggest that Hog1 regulates biofilm formation by T. asahii in response to host environmental conditions, including oxidative stress.