Abstract
Botrytis cinerea is one of the most destructive ascomycete pathogens affecting crops worldwide and causing severe yield losses. Broad-spectrum fungicides are used to control fungal pathogenic diseases, but pathogens develop resistance toward these fungicides through point mutations. In this study, we isolated and observed resistance mechanisms in B. cinerea. All five isolates considered in this study belonged to this pathogen species, which affects tomato fruits. The phenotypic resistance profile was analyzed in terms of specific resistance to multiple succinate dehydrogenase inhibitors (SDHI) and benzimidazole-based fungicides (boscalid, Bos(R), flypyram, Flu(R), carbendazim, Car(MR)), (Bos(R)Flu(MR)Car(MR)), (Bos(MR)Flu(R)Car(R)), (Bos(MR)Flu(MR)Car(MR)) (Bos(S)Flu(S)Car(S)). The Half maximal effective concentration (EC50) (mu g/mL) value ranges were 1.10-3.51 forboscalid-resistant isolates, 1.05-2.25 for fluopyram-resistant isolates, and 0.89-3.82 for carbendazim-resistant isolates. To investigate the molecular mechanism of resistance, the Sdh-B and beta-tubulin genes of the respective SDHI-resistant and carbendazim-resistant isolates were amplified, and their amino acid sequences were compared with those of sensitive strains. The SDHI-resistant isolate of B. cinerea showed mutations G282A and G372V, while the carbendazim-resistant one presented mutation E947A. Integrated disease management and the application of new fungicides with low resistance risk should be implemented in order to reduce the risk of resistance development in B. cinerea.