FSH1 regulates the phenotype and pathogenicity of the pathogenic dermatophyte Microsporum canis

Furong Zhang1, Can Tan1, Yu Xu2

  • 1Department of Dermatology, The First Affiliated Hospital of Dalian Medical University, Chengdu, Sichuan 11736, P.R. China.

Insights

Family of serine hydrolases 1 (FSH1) is crucial for Microsporum canis virulence and macroconidia septa formation. Knocking down FSH1 reduced M. canis pathogenicity in guinea pig infections, highlighting its role in fungal infections.

Area of Science:

  • Mycology
  • Medical Microbiology
  • Molecular Biology

Background:

  • Microsporum canis (M. canis) is a globally prevalent pathogen causing tinea capitis, with rising incidence in China.
  • Previous research identified the family of serine hydrolases 1 (FSH1) as a potential virulence factor in M. canis infections.

Purpose of the Study:

  • To elucidate the functional role of the FSH1 gene in M. canis.
  • To investigate the association of FSH1 with macroconidia septa formation and M. canis pathogenicity.

Main Methods:

  • Gene knockdown of FSH1 in M. canis using Agrobacterium tumefaciens-mediated double-stranded RNA interference.
  • Confirmation of gene knockdown via reverse transcription-quantitative PCR (RT-qPCR).
  • Assessment of M. canis pathogenicity through guinea pig cutaneous infection models.

Main Results:

  • RNA interference-mediated knockdown of FSH1 resulted in minimal phenotypic alterations in M. canis.
  • Reduced M. canis pathogenicity was observed in guinea pig models following FSH1 knockdown compared to wild-type strains.
  • FSH1 was identified as being associated with macroconidia septa formation in M. canis.

Conclusions:

  • The study demonstrates that FSH1 is a significant contributor to M. canis virulence.
  • FSH1 plays a role in the formation of macroconidia septa.
  • These findings provide a foundation for understanding FSH1's function and M. canis pathogenicity.

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