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Background <p>Verticillium wilt (VW), a devastating disease caused by the soil-inhabiting fungus <i>Verticillium dahliae</i>, poses a substantial threat to cotton cultivation worldwide by drastically impairing both yield and fiber quality. Although C₂H₂ zinc finger proteins (ZFPs) are known regulators of plant stress responses, their role in cotton immunity against <i>V. dahliae</i> remains largely unexplored.</p> Results <p>Here, we identified the C₂H₂ ZFP gene <i>GhBsr-d1L7</i> through homology-based approaches, and investigated its function in disease resistance in upland cotton. Silencing <i>GhBsr-d1L7</i> using virus-induced gene silencing (VIGS) rendered cotton plants more susceptible to <i>V. dahliae</i>, as evidenced by reduced levels of reactive oxygen species (ROS), jasmonic acid (JA), lignin, and decreasing Catalase (CAT) activity. Conversely, heterologous overexpression of <i>GhBsr-d1L7</i> in Arabidopsis enhanced resistance and activated associated defense responses. Transcriptome analysis indicated that silencing <i>GhBsr-d1L7</i> altered the expression profiles of genes associated with hormone signaling, phenylpropanoid biosynthesis, and MAPK cascades. In addition, yeast two-hybrid screening identified GhERD10, a dehydrin-family protein, as a nuclear interactor of GhBsr-d1L7, with this interaction validated by luciferase complementation imaging and bimolecular fluorescence complementation assays. Notably, silencing <i>GhERD10</i> significantly enhanced cotton resistance to <i>V. dahliae</i>, implicating its role as a negative regulator of plant immunity.</p> Conclusions <p>Together, these findings reveal a novel C₂H₂ ZFP-chaperone module (GhBsr-d1L7-GhERD10) that integrates physiological and transcriptional defenses to bolster cotton immunity. This study deepens our understanding of plant-pathogen interactions and identifies promising molecular targets for developing disease-resistant cotton varieties.</p>

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An integrative defense mechanism mediated by GhBsr-d1L7 and GhERD10 confers resistance to Verticillium dahliae in cotton

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月27日

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  • Guoshuai Zhang,
  • Chuanzong Li,
  • Youzhong Li,
  • Zongming Xie,
  • Yanqing Bi,
  • Xinyu Zhu,
  • Jianfeng Lei,
  • Peihong Dai,
  • Xiaofeng Su,
  • Yue Li

摘要

Background

Verticillium wilt (VW), a devastating disease caused by the soil-inhabiting fungus Verticillium dahliae, poses a substantial threat to cotton cultivation worldwide by drastically impairing both yield and fiber quality. Although C₂H₂ zinc finger proteins (ZFPs) are known regulators of plant stress responses, their role in cotton immunity against V. dahliae remains largely unexplored.

Results

Here, we identified the C₂H₂ ZFP gene GhBsr-d1L7 through homology-based approaches, and investigated its function in disease resistance in upland cotton. Silencing GhBsr-d1L7 using virus-induced gene silencing (VIGS) rendered cotton plants more susceptible to V. dahliae, as evidenced by reduced levels of reactive oxygen species (ROS), jasmonic acid (JA), lignin, and decreasing Catalase (CAT) activity. Conversely, heterologous overexpression of GhBsr-d1L7 in Arabidopsis enhanced resistance and activated associated defense responses. Transcriptome analysis indicated that silencing GhBsr-d1L7 altered the expression profiles of genes associated with hormone signaling, phenylpropanoid biosynthesis, and MAPK cascades. In addition, yeast two-hybrid screening identified GhERD10, a dehydrin-family protein, as a nuclear interactor of GhBsr-d1L7, with this interaction validated by luciferase complementation imaging and bimolecular fluorescence complementation assays. Notably, silencing GhERD10 significantly enhanced cotton resistance to V. dahliae, implicating its role as a negative regulator of plant immunity.

Conclusions

Together, these findings reveal a novel C₂H₂ ZFP-chaperone module (GhBsr-d1L7-GhERD10) that integrates physiological and transcriptional defenses to bolster cotton immunity. This study deepens our understanding of plant-pathogen interactions and identifies promising molecular targets for developing disease-resistant cotton varieties.