Abstract Sclerotinia stem rot caused by Sclerotinia sclerotiorum severely constrains global crop production. This study explored the regulatory role of checkpoint kinase SsChk2 in tebuconazole resistance. Bioassays indicated that ΔSsChk2 mutants showed reduced sensitivity to three demethylation inhibitors (DMIs), compared with wild-type strain UF-1, while maintaining normal biological phenotypes. Transcription of SsChk2 was significantly suppressed in five UV-induced tebuconazole-resistant mutants and inhibitor-treated UF-1. Independent of SsCYP51 amino acid substitutions, the ΔSsChk2 strain exhibited elevated SsCYP51 expression, ergosterol accumulation, and cellular structural stability under tebuconazole stress. RNA-seq analyses revealed that SsChk2 deletion upregulated key ergosterol biosynthesis genes and ABC1/MFS2 transporters and activated coordinated defensive pathways. These findings reveal that loss or downregulation of SsChk2 stimulates ergosterol biosynthesis to confer DMI resistance and uncover a promising target for sustainable control of Sclerotinia stem rot.
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