Key result
Deleting the cnb1 gene in Trichosporon asahii attenuates pathogenicity, increasing LD50 ~89-fold in silkworms.
Why the study?
Elucidating the infection mechanisms of the pathogenic fungus Trichosporon asahii based on genetic studies requires a specific gene-targeting system.
An efficient gene-targeting system was established in a highly pathogenic T. asahii strain, providing a useful tool for elucidating its infection mechanisms.
Establishes a gene-targeting tool in pathogenic T. asahii; leaves open its utility for human infection mechanism studies.
Trichosporon asahii is a pathogenic fungus that causes severe, deep-seated fungal infections in neutropenic patients. Elucidating the infection mechanisms of T. asahii based on genetic studies requires a specific gene-targeting system. Here, we established an efficient gene-targeting system in a highly pathogenic T. asahii strain identified using the silkworm infection model. By comparing the pathogenicity of T. asahii clinical isolates in a silkworm infection model, T. asahii MPU129 was identified as a highly pathogenic strain. Using an Agrobacterium tumefaciens-mediated gene transfer system, we obtained a T. asahii MPU129 mutant lacking the ku70 gene, which encodes the Ku70 protein involved in the non-homologous end-joining repair of DNA double-strand breaks. The ku70 gene-deficient mutant showed higher gene-targeting efficiency than the wild-type strain for constructing a mutant lacking the cnb1 gene, which encodes the beta-subunit of calcineurin. The cnb1 gene-deficient mutant showed reduced pathogenicity against silkworms compared with the parental strain. These results suggest that an efficient gene-targeting system in a highly pathogenic T. asahii strain is a useful tool for elucidating the molecular mechanisms of T. asahii infection.
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Matsumoto et al. (2021) studied Trichosporon asahii infection (silkworm model). ku70 and cnb1 gene deletion vs. Wild-type T. asahii MPU129 strain was evaluated on Pathogenicity (LD50) in silkworms. Deletion of the ku70 gene in Trichosporon asahii increased gene-targeting efficiency, enabling the creation of a cnb1 gene-deficient mutant that showed an 89-fold higher LD50 and attenuated pathogenicity in a silkworm model.
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