Fusarium graminearum possesses virulence factors common to Fusarium head blight of wheat and seedling rot of soybean, but differing in their impact on disease severity.

Fusarium graminearum is a toxigenic fungal pathogen which causes Fusarium head blight (FHB) and crown rot (CR) on cereal crops worldwide. This fungus also causes damping off and crown and root rots at the early stage of crop development in soybean cultivated in North and South America. Several F. graminearum genes were investigated for their contribution to FHB in cereals but no inherent study is reported for the dicotyledonous soybean host. In this study we determined the disease severity on soybean seedlings of five single gene disrupted mutants of F. graminearum, previously characterized in wheat spike infection. Three of these mutants are impaired on a specific function as the production of deoxynivalenol (DON, ∆tri5), lipase (ΔFgl1) and xylanase (∆xyl03624), while the remaining two are MAP kinase mutants (ΔFgOS-2, ∆gpmk1) which are altered in signaling pathways. The mutants that were reduced in virulence (Δtri5, ΔFgl1 and ΔFgOS-2) or avirulent (Δgpmk1) on wheat, were correspondently less virulent or avirulent in soybean seedlings, as shown by the extension of lesions and seedling lengths. The ∆xyl03624 mutant was as virulent as the WT mirroring the behavior observed in wheat. However, a different ranking of symptom severity occurred in the two hosts: the ΔFgOS-2 mutant, that infects wheat spikelets similarly to Δtri5 and ΔFgl1 mutants, gave much reduced symptoms in soybean. Differently from the other mutants, we observed that the ΔFgOS-2 mutant was several fold more sensitive to the glyceollin phytoalexin suggesting that its reduced virulence may be due to its hypersensitivity to this phytoalexin. In conclusion, lipase and DON seem important for full disease symptoms development in soybean seedlings, OS-2 and Gpmk1 MAP kinases are essential for virulence, and OS-2 is involved in conferring resistance to the soybean phytoalexin.