The MFS transporter BcTpo1 governs the oxidative stress response and infection of Botrytis cinerea

Lingchao Wang1, Youmei Xie1, Jiaxuan Li1

  • 1Shandong Provincial Key Laboratory of Microbial Resource Exploration and Innovative Utilization, Engineering Research Center for Precision Pest Management for Fruits and Vegetables of Qingdao, College of Plant Health and Medicine, Shandong Engineering Research Center for Environment-Friendly Agricultural Pest Management, Qingdao Agricultural University, Qingdao, China.

Crop Health
|April 22, 2026
PubMed

Insights

Spermine inhibits gray mold pathogen Botrytis cinerea. Its transporter, BcTpo1, is crucial for virulence, linking spermine levels to oxidative stress and pathogenicity.

Area of Science:

  • Plant Pathology
  • Mycology
  • Molecular Biology

Background:

  • Botrytis cinerea causes gray mold, a significant plant disease.
  • Understanding fungal pathogenicity is key to developing control strategies.

Purpose of the Study:

  • Investigate the role of spermine and its transporter BcTpo1 in Botrytis cinerea virulence.
  • Determine how BcTpo1 affects fungal growth, stress response, and pathogenicity.

Main Methods:

  • Gene deletion of BcTpo1 in Botrytis cinerea.
  • Assessing fungal growth, conidiation, sclerotia formation, and melanin production.
  • Evaluating response to oxidative stress and infection structure formation.

Main Results:

  • Spermine, not spermidine, inhibited conidial germination and pathogenicity.
  • BcTpo1 deletion caused defects in growth, conidiation, sclerotia, and melanin.
  • ΔBcTpo1 strains showed reduced spermine, increased H2O2 sensitivity, and impaired infection structures.
  • Exogenous spermine partially rescued ΔBcTpo1 defects by boosting antioxidant enzymes.

Conclusions:

  • BcTpo1 is essential for fungal virulence in Botrytis cinerea.
  • BcTpo1 regulates spermine homeostasis, impacting oxidative stress adaptation.
  • This transporter links spermine metabolism to pathogenicity in this important plant pathogen.

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