A new point mutation in β2-tubulin confers resistance to carbendazim in Fusarium asiaticum

Abstract 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 β 2 -tubulin that confers resistance to carbendazim and to analyze the molecular interaction between carbendazim and F. asiaticum β 2 -tubulin. In this study, a new point mutation (GAG → GCG, E198A) at codon 198 of β 2 -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 β 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 β 2 -tubulin, resulting in the change of the bonding sites and docking scores. We concluded that the point mutation of F. asiaticum β 2 -tubulin conferring carbendazim resistance may not always be the bonding site for carbendazim.