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Background <p><i>Nicotiana tabacum</i> is a high-value economic crop with medicinal uses. Tobacco leaf spot disease, caused by <i>Corynespora cassiicola</i>, severely reduces yield and quality, threatening tobacco production. Benzimidazole fungicides are commonly used, but <i>C. cassiicola</i> has developed resistance, creating an urgent need for new fungicides.</p> Results <p>This study investigated the inhibitory mechanism and control potential of JNK inhibitor SP600125 against <i>C. cassiicola</i> in tobacco. Mycelial growth assays showed SP600125 significantly inhibited growth, with an EC₅₀ of 446.8 µM. At this concentration, colony diameter was 47.9% ± 1.5% of the control, and necrotic leaf spots reduced to 52.1% of control. Scanning electron microscopy revealed thinner, malformed hyphae. Transcriptome analysis showed altered expression of genes linked to biological processes, cellular components, and molecular functions. We identified 25 MAPK pathway genes after 24&#xa0;h SP600125 treatment, 35 after 48&#xa0;h.</p> Conclusion <p>In summary, this study indicates that SP600125 impairs <i>C. cassiicola</i> hyphal structure and growth, with transcriptomic data suggesting potential involvement of JNK/MAPK pathway-related genes. While its high EC₅₀ limits direct application as a commercial fungicide, SP600125 serves as a valuable biological probe to dissect fungal JNK/MAPK signaling and holds potential as a candidate fungicide following formulation optimization or combination strategies. Direct evidence of JNK inhibition, however, remains to be confirmed.</p>

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Transcriptomic and phenotypic responses of Corynespora cassiicola to the JNK inhibitor SP600125

  • 期刊论文

  • 发表日期：

    2026年4月22日

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  • Chunyang Huang,
  • Kelin Jin,
  • Yanjie Chen,
  • Zhaolan Ma,
  • Lu Cai,
  • Jingrong Hu,
  • Dongfang Ma

摘要

Background

Nicotiana tabacum is a high-value economic crop with medicinal uses. Tobacco leaf spot disease, caused by Corynespora cassiicola, severely reduces yield and quality, threatening tobacco production. Benzimidazole fungicides are commonly used, but C. cassiicola has developed resistance, creating an urgent need for new fungicides.

Results

This study investigated the inhibitory mechanism and control potential of JNK inhibitor SP600125 against C. cassiicola in tobacco. Mycelial growth assays showed SP600125 significantly inhibited growth, with an EC₅₀ of 446.8 µM. At this concentration, colony diameter was 47.9% ± 1.5% of the control, and necrotic leaf spots reduced to 52.1% of control. Scanning electron microscopy revealed thinner, malformed hyphae. Transcriptome analysis showed altered expression of genes linked to biological processes, cellular components, and molecular functions. We identified 25 MAPK pathway genes after 24 h SP600125 treatment, 35 after 48 h.

Conclusion

In summary, this study indicates that SP600125 impairs C. cassiicola hyphal structure and growth, with transcriptomic data suggesting potential involvement of JNK/MAPK pathway-related genes. While its high EC₅₀ limits direct application as a commercial fungicide, SP600125 serves as a valuable biological probe to dissect fungal JNK/MAPK signaling and holds potential as a candidate fungicide following formulation optimization or combination strategies. Direct evidence of JNK inhibition, however, remains to be confirmed.