The gray mold caused by Botrytis cinerea has a significant impact on tomato production throughout the world. Although the synthetic fungicide
fludioxonil can effectively control B. cinerea, there have been several reports of resistance to this fungicide. This study indicated that all of the
fludioxonil-resistant strains tested, including one field-resistant isolate and four laboratory strains, had reduced fitness relative to sensitive isolates. In addition to having reduced growth, sporulation, and pathogenicity, the resistant strains were more sensitive to osmotic stress and had significantly (P < 0.05) higher
peroxidase activity.
BOs1, a
kinase in the high-osmolarity
glycerol stress response signal transduction pathway, is believed to harbor mutations related to
fludioxonil resistance. Sequence analysis of their
BOs1 sequences indicated that the
fludioxonil-resistant field isolate, XXtom1806, had four point mutations resulting in four
amino acid changes (I365S, S531G, T565N, and T1267A) and three
amino acids (I365S, S531G, and T565N) in the
histidine kinases,
adenylyl cyclases, methyl-accepting chemotaxis receptors, and
phosphatases domain, which associated with
fludioxonil binding. Similarly, two of the laboratory strains, XXtom-Lab1 and XXtom-Lab4, had three (Q846S, I1126S, and G415D) and two (P1051S and V1241M) point mutations, respectively. A third strain, XXtom-lab3, had a 52-bp insertion that included a stop
codon at
amino acid 256. Interestingly, the
BOs1 sequence of the fourth laboratory strain, XXtom-lab5, was identical to those of the sensitive isolates, indicating that an alternative resistance mechanism exists. The study also found evidence of positive cross-resistance between
fludioxonil and the dicarboximide fungicides
procymidone and
iprodione, but no cross-resistance was detected with any other fungicides tested, including
boscalid,
carbendazim,
tebuconazole, and
fluazinam.