Molecular mechanism of resistance of Fusarium fujikuroi to benzimidazole fungicides
2014
Chen, Zihao | Gao, Tao | Liang, Shuping | Liu, Kexue | Zhou, Mingguo | Chen, Changjun
Although carbendazim (MBC) and other benzimidazole fungicides have effectively controlled bakanae disease of rice (which is caused by Fusarium fujikuroi, F. proliferatum, and F. verticillioides) in the past, MBC resistance has become common. Previous research has shown that MBC resistance results from a mutation in the β₁‐tubulin (β₁tub) gene in F. verticillioides. However, MBC resistance in F. fujikuroi, a predominant species in China, does not result from a mutation in the β₁tub. The molecular mechanism of F. fujikuroi resistance against benzimidazole fungicides is poorly understood. In this study, we determined that although β₁tub and β₂‐tubulin (β₂tub) in F. fujikuroi have high homology with β₁tub and β₂tub in F. verticillioides, MBC resistance in F. fujikuroi results from mutations in β₂tub [GAG(Glu)→GTG(Val) at codon 198, TTC(Phe)→TAC(Tyr) at codon 200, and GGC(Gly)→GGT(Gly) at codon 235] but not in β₁tub. Δβ₂tub (β₂tub deletion) mutants were highly sensitive to MBC, produced fewer conidia and were less virulent than parental strains. Complementation of the Δβ₂tub mutants with a copy of the whole β₂tub locus from their parental strains restored the level of MBC resistance (or sensitivity) to that of the parental strain.
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