Involvement of FgMad2 and FgBub1 in regulating fungal development and carbendazim resistance in Fusarium graminearum

Resistance to carbendazim of Fusarium graminearum is conferred by point mutation in the beta(2)-tubulin gene that plays an important role in spindle assembly. The spindle assembly checkpoint is a cellular surveillance system that is critical for maintaining genomic stability. Predicted protein Mad2- and Bub1-encoding genes in F. graminearum (FgMad2 and FgBub1) were isolated and characterized. There was no difference in FgMad2 and FgBub1 expression levels between carbendazim-sensitive and -resistant strains; however, after carbendazim treatment FgMad2 expression increased while FgBub1 expression stayed the same. Both the FgMad2 and FgBub1 deletion mutants became more sensitive to carbendazim. The FgMad2 deletion mutants grew more slowly, produced fewer conidia and both hyphae and conidia were malformed. Conversely, deletion of FgBub1 had no effect on fungal development other than a reduction in conidia production. FgMad2 deletion mutants exhibited a severe decrease in perithecia production and pathogenicity along with a down-regulation of trichothecene production, whereas FgBub1 deletion mutants exhibited only a slight reduction in perithecia production and was accompanied by a twofold increase in trichothecene production. Overall, the results indicate that both FgMad2 and FgBub1 are involved in carbendazim resistance and trichothecene biosynthesis, and FgMad2 plays an important role in fungal development in F. graminearum.