ABSTRACT
摘要
Brown rot, caused by Monilinia fructicola, is the most destructive pre- and postharvest fruit rot of peach worldwide. In 2024, a disease outbreak occurred in a South Carolina orchard despite a rigorous chemical management program consisting of preharvest applications of SDHI, QoI, and DMI fungicides. Isolates from affected orchards carried the Mona element upstream of the MfCYP51 gene, associated with reduced DMI fungicide sensitivity in the southeastern region. They displayed low, moderate, or high levels of resistance to boscalid, isofetamid, fluopyram, and fluxapyroxad based on EC 50 values ranging from 0.33 to >300, 0.22 to 1.95, 0.28 to 7.41 and 0.30 to 115.11 µg/ml, respectively. In contrast, EC 50 values obtained for historic isolates were ≤ 0.05 µg/ml for all SDHI fungicides. Whole-genome sequencing identified five SDH genotypes: wild type (WT; no aa substitutions); G1 (N226H in SDHB); G2 (P80H in SDHC); G3 (N226H in SDHB + V26I in SDHD); and G4 (N226H in SDHB, P80H in SDHC, and T24A in SDHD). Isolates harboring aa changes in multiple SDH subunits had the highest EC 50 values and were resistant to all SDHIs tested. Detached fruit assays confirmed that label rates of SDHI fungicides failed to control isolates carrying multiple aa changes. To the best of our knowledge, this study provides the first report worldwide of SDHI resistance in Monilinia species field isolates linked to aa changes in the SDH subunits and combined SDHI and DMI resistance in peach orchards, highlighting the need for resistance monitoring and management.