ArticleScientific reports2023
Hog1-mediated stress tolerance in the pathogenic fungus Trichosporon asahii.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- Magnesium enhances the expression of arthroconidia-related genes inMicrobiology spectrum · 2026Article
- Calcineurin-responsive zinc finger 1 (Crz1) contributes to stress tolerance and virulence in the pathogenic fungusInfection and immunity · 2026Article
- Functional characteristics and distribution of microorganisms in saline and alkaline soils and their probiotic effects: a review.Microbial cell factories · 2026Review
- Trichosporon and Antifungal Resistance: Current Knowledge and Gaps.Mycopathologia · 2025Review
- Identification of the ADH gene family in Trichosporon asahii and the role of TaADH_like in pathogenicity and fluconazole resistance.BMC genomics · 2025Article
- Pathogenic characterization ofFrontiers in cellular and infection microbiology · 2025Article
- Role of Hog1-mediated stress tolerance in biofilm formation by the pathogenic fungus Trichosporon asahii.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trichosporon asahii is an opportunistic pathogenic fungus that causes severe and sometimes fatal infections in immunocompromised patients. Hog1, a mitogen-activated protein kinase, regulates the stress resistance of some pathogenic fungi, however 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. 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 hog1 gene-deficient mutant against silkworms was attenuated. Moreover, the viability of the hog1 gene-deficient mutant 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 plays a critical role in regulating cellular stress responses in T. asahii.
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Registered trials
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