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<p><i>Botrytis cinerea</i>&#xa0;is a devastating necrotrophic pathogen causing gray mold disease. Understanding its pathogenic mechanisms is critical for developing novel control strategies. In this study, we investigated the role of spermine and its transporter BcTpo1 in fungal virulence. Spermine, but not spermidine, specifically inhibited conidial germination, infection structure formation, and pathogenicity. Deletion of&#xa0;<i>BcTpo1</i>&#xa0;resulted in pleiotropic defects, including altered mycelial growth, conidiation, sclerotia formation, and melanin biosynthesis. Under oxidative stress, Δ<i>BcTpo1</i>&#xa0;exhibited reduced intracellular spermine levels compared to the wild-type strain, correlating with elevated hydrogen peroxide sensitivity and impaired infection cushion formation. Exogenous spermine partially rescued these defects by enhancing antioxidant enzyme (superoxide dismutase and peroxidase) activities. Together, these findings establish BcTpo1 as a key regulator linking spermine homeostasis, oxidative stress adaptation, and pathogenicity.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年4月22日

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  • Lingchao Wang,
  • Youmei Xie,
  • Jiaxuan Li,
  • Fugen Yang,
  • Wenxing Liang,
  • Qianqian Yang

摘要

Botrytis cinerea is a devastating necrotrophic pathogen causing gray mold disease. Understanding its pathogenic mechanisms is critical for developing novel control strategies. In this study, we investigated the role of spermine and its transporter BcTpo1 in fungal virulence. Spermine, but not spermidine, specifically inhibited conidial germination, infection structure formation, and pathogenicity. Deletion of BcTpo1 resulted in pleiotropic defects, including altered mycelial growth, conidiation, sclerotia formation, and melanin biosynthesis. Under oxidative stress, ΔBcTpo1 exhibited reduced intracellular spermine levels compared to the wild-type strain, correlating with elevated hydrogen peroxide sensitivity and impaired infection cushion formation. Exogenous spermine partially rescued these defects by enhancing antioxidant enzyme (superoxide dismutase and peroxidase) activities. Together, these findings establish BcTpo1 as a key regulator linking spermine homeostasis, oxidative stress adaptation, and pathogenicity.