Role of Atg1 in morphologic changes of the pathogenic fungus Trichosporon asahii

Trichosporon asahii is a dimorphic fungus that causes severe invasive fungal infections, particularly in patients with neutropenia. Depending on nutrient availability, T. asahii exists in yeast, hyphae, or arthroconidia forms. Autophagy, a cellular degradation pathway that removes old or damaged organelles, is essential for the survival of many eukaryotic organisms under nutrient-limited conditions. Atg1 is a key regulator of the early phases of autophagy, especially under nitrogen starvation. The role of Atg1 in regulating morphology, stress resistance, or virulence in T. asahii , however, remains poorly understood. Here, we generated three atg1 gene-deficient T. asahii mutants and investigated their phenotypic characteristics to reveal the role of Atg1 in T. asahii . The atg1 gene-deficient mutants exhibited no growth defects under high-temperature or various chemical stress conditions, including antifungal drugs. The mutants exhibited an increased proportion of hyphal cells when cultured in Sabouraud dextrose broth (SB), a medium commonly used for fungi. On the other hand, no morphologic differences were observed between the parent strain and the atg1 gene-deficient mutants under a nitrogen-limited condition. The virulence of these atg1 gene-deficient mutants was maintained in a silkworm infection model. Furthermore, all three generated atg1 gene-deficient mutants exhibited consistent phenotypes. Our findings suggest that while Atg1 does not play a major role in stress tolerance or virulence in T. asahii , it plays a role in regulating its dimorphic morphologic changes.