Abstract:

Fusarium head blight (FHB) caused by Fusarium graminearum is a devastating disease of wheat, barley, oats, rye, and other cereal crops. Currently, the control of FHB in production mainly depends on chemical agents, among which carbendazim and other benzimidazole fungicides are widely used. The target of these fungicides is β-tubulin. There are two β tubulins in F. graminearum. A previous study showed that the 138th amino acid of β2-tubulin might be a carbendazim binding site. In this study, a Fgβ2 Ser138 mutation was constructed to clarify its biological function. The results showed that the sensitivity of Fgβ2 S138Amutation to carbendazim was significantly increased, and the EC₅₀ value decreased from 0.617 mg/L to about 0.290 mg/L, however, the mutations did not affect the sensitivity to thiabendazole, and the EC₅₀ value was about 0.950 mg/L, and all of them did not affect the vegetative growth, asexual reproduction, sexual reproduction and pathogenicity of F. graminearum. These results provide a theoretical basis for the chemical control of carbendazim against FHB and have a particular guiding significance in production.

Key words: Fusarium graminearum; Fusarium head blight, fungicide sensitivity; site-directed mutagenesis