Succinate dehydrogenase inhibitor (SDHI) fungicides have a wide spectrum of fungicidal effects on a variety of fungi causing plant diseases, including Sclerotinia stem rot caused by Sclerotinia sclerotiorum. However, the consistent use of site-specific SDHI fungicides can result in the development of resistant isolates with mutations in the SDHB, SDHC, or SDHD subunit thereby leading to a rapid decline of fungicide performance. In this study, we found that SDHC was genetically evolved into two isotypes SDHC1 and SDHC2 in S. sclerotiorum but not involved in the sensitivity to SDHI fungicides. In addition, we demonstrated that the A11V substitution in SDHB was not involved in the resistance of S. sclerotiorum to boscalid, and this substitution widely emerged in the field populations. Meanwhile, the P226L substitution in SDHB was demonstrated to confer boscalid resistance in S. sclerotiorum. The result of cross-resistance showed that the SDHB-P226L substitution exhibited a positive cross-resistance between boscalid and carboxin, fluopyram, pydiflumetofen, flubeneteram, pyraziflumid, fluindapyr, or penthiopyrad. Taken together, our results indicated that the P226L substitution in SDHB resulted in the resistance of S. sclerotiorum to SDHI fungicides but suffered from fitness penalty, especially the homozygous mutants conferring the P226L substitution in SDHB.
Keywords: SDHB-P226L; SDHI fungicides; Sclerotinia sclerotiorum; resistance mechanism.