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.