Hog1-mediated stress tolerance in the pathogenic fungus Trichosporon asahii

Abstract

Abstract Trichosporon asahii is a conditional pathogenic fungus that causes severe and sometimes fatal infections in immunocompromised patients.Hog1, a mitogen-activated protein kinase, is known to regulate the stress resistance of some pathogenic fungi, but its role in T. asahii has not been investigated. Here, we demonstrated that the hog1 gene-deficient T. asahii mutant is sensitive to high temperature, cell-membrane stress, oxidative stress, and antifungal drugs. The growth of the hog1 gene-deficient T. asahii mutant was delayed at 40˚C. The hog1 gene-deficient T. asahii mutant also exhibited sensitivity to sodium dodecyl sulfate, hydrogen peroxide, menadione, methyl methanesulfonate, UV exposure, and antifungal drugs such as amphotericin B under a glucose-rich condition. Under a glucose-restricted condition, the hog1 gene-deficient mutant exhibited sensitivity to NaCl and KCl. The virulence of the hog1gene-deficient mutant against silkworms was attenuated. Moreover, the cell viability of the hog1 gene-deficient mutant was decreased in the silkworm hemolymph. These phenotypes were restored by re-introducing the hog1 gene into the gene-deficient mutant. Our findings suggest that Hog1 has a critical role in regulating the cellular stress responses of T. asahii.