Molecular Mechanism of <i>Sclerotinia sclerotiorum</i> Resistance to Succinate Dehydrogenase Inhibitor Fungicides

Abstract

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 <i>Sclerotinia sclerotiorum</i>. 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 <i>S. sclerotiorum</i> 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 <i>S. sclerotiorum</i> to boscalid, and this substitution widely emerged in the field populations. Meanwhile, the P226L substitution in SDHB was demonstrated to confer boscalid resistance in <i>S. sclerotiorum</i>. 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 <i>S. sclerotiorum</i> to SDHI fungicides but suffered from fitness penalty, especially the homozygous mutants conferring the P226L substitution in SDHB.