Resistance to benzimidazole fungicides in many phytopathogenic fungi is caused by specific point mutations in the β-tubulin gene (β-tubulin). However, the mutated locus and genotype of β-tubulin differ among phytopathogenic fungi. To validate the point mutation in Fusarium asiaticum β2-tubulin that confers resistance to carbendazim and to analyze the molecular interaction between carbendazim and F. asiaticum β2-tubulin. In this study, a new point mutation (GAG→GCG, E198A) at codon 198 of β2-tubulin in a wild-type F. asiaticum strain was constructed by site-directed mutagenesis followed by a split marker strategy. The site-directed mutants were verified and exhibited a high level of resistance to carbendazim. In the absence of fungicide treatment, the biological characteristics did not differ between the site-directed mutants and the wild-type strain. Molecular docking between carbendazim and β2-tubulin was carried out using the Surflex-Dock program in Sybyl X-2.0 version and the results indicated that the E198A mutation altered the configuration of β2-tubulin, resulting in the change of the bonding sites and docking scores. We concluded that the point mutation of F. asiaticum β2-tubulin conferring carbendazim resistance may not always be the bonding site for carbendazim.
Keywords: Carbendazim; Fusarium asiaticum; Resistance; Site-directed mutagenesis; β-tubulin.
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