Wheat transgenic plants expressing a bean PGIP support a role for polygalacturonase activity in the initial stage of wheat infection by Fusarium graminearum

Fusarium graminearum is one of the predominant causal agents of Fusarium Head Blight (FHB) of wheat worldwide. This fungal pathogen produces trichothecene mycotoxins, including deoxynivalenol (DON). Transgenic wheat plants expressing the FsTRI101 gene, which encodes a DON acetyltransferase, were partially protected against the spread of F. graminearum. F. graminearum also secretes an array of enzymes to degrade cell wall polymers. Since some of these enzymes are controlled by apoplastic inhibitor proteins, we are analyzing the feasibility of increasing host resistance by manipulating the activity of these cell wall components. We report the effect of the ectopic expression of a bean polygalacturonase-inhibiting protein (PvPGIP2) in transgenic wheat plants, alone and in combination with the product of the FsTri101 gene, in protecting wheat plants against F. graminearum. We monitor FHB symptom progression in inoculated heads for 23 days. We show that transgenic plants expressing PvPGIP2 show a significant reduction of FHB symptoms from 9 to 23 dpi. A parallel analysis performed on wheat transgenic lines expressing FsTri101 showed a delayed protective effect starting from 15 to 23 dpi. We also evaluated the effects of combining the Pvpgip2 and FsTRI101 transgenes on the spread of the FHB symptoms. The hybrid lines carrying both transgenes show symptom reductions equal to either parental line, but an earlier reduction of FHB symptoms (from 11 to 23 dpi) than the parental line expressing only FsTRI101. These results demonstrate that PvPGIP2 can slow Fusarium infection and support a role for polygalacturonase activity in the initial stage of colonization