Fumarylacetoacetate hydrolase targeted by a Fusarium graminearum effector positively regulates wheat FHB resistance.

Abstract

Fusarium head blight (FHB), caused by Fusarium graminearum is a devastating disease that affects global wheat production. F. graminearum encodes many effector proteins; however, its virulence mechanisms are poorly understood. In this study, we identify a secretory effector candidate (FgEC10) that is essential for the virulence of F. graminearum. FgEC10 interacts strongly with wheat fumarylacetoacetate hydrolase (TaFAH) and accelerates its degradation via the 26S proteasome pathway. In addition, we show that TaFAH interacts with proteasome 26S subunit, non-ATPases 12 (TaPSMD12) and that FgEC10 enhances the interaction between TaFAH and TaPSMD12. RNA silencing or overexpression of TaFAH in wheat plants shows that TaFAH positively regulates wheat FHB resistance. Overexpression of TaFAH promotes the expression of genes associated with disease resistance and the heading period. Metabolomic analysis reveals that overexpression of TaFAH increases the levels of several amino acids in wheat, and exogenous application of some of these amino acids show an increase in F. graminearum resistance in the wheat spike and seedling. Collectively, our study reveals a pathogenic mechanism and provides a valuable gene resource for improving FHB resistance and promoting heading in wheat.