A new point mutation in beta(2)-tubulin confers resistance to carbendazim in Fusarium asiaticum

Resistance to benzimidazole fungicides in many phytopathogenic fungi is caused by specific point mutations in the beta-tubulin gene (beta-tubulin). However, the mutated locus and genotype of beta-tubulin differ among phytopathogenic fungi. To validate the point mutation in Fusarium asiaticum beta(2)-tubulin that confers resistance to carbendazim and to analyze the molecular interaction between carbendazim and F. asiaticum beta(2)-tubulin. In this study, a new point mutation (GAG -> GCG, E198A) at codon 198 of beta(2)-ruhulin 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 beta(2)-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 beta(2)-tubulin, resulting in the change of the bonding sites and docking scores. We concluded that the point mutation of F. asiaticum beta(2)-tubulin conferring carbendazim resistance may not always be the bonding site for carbendazim.