Fusarium graminearum is a toxigenic fungal pathogen that causes Fusarium head 
blight (FHB) and crown rot 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, Δtri5), lipase (ΔFgl1), and xylanase (Δxyl03624), while the 
remaining two are MAP kinase mutants (ΔFgOS-2, Δgpmk1), which are altered in 
signaling pathways. The mutants that were reduced in virulence (Δtri5, ΔFgl1, 
and ΔFgOS-2) or are avirulent (Δgpmk1) on wheat were correspondently less 
virulent or avirulent in soybean seedlings, as shown by the extension of lesions 
and seedling lengths. The Δxyl03624 mutant was as virulent as the wild type 
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, provided 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 
symptom 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.