ArticleMolecular biology reports2026
Transcriptomic and phenotypic responses of Corynespora cassiicola to the JNK inhibitor SP600125.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundNicotiana 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.
resultsThis 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.
conclusionIn 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.
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