An RGAE Homolog in Fusarium graminearum Is Critical for Initial Infection in Wheat and Barley.

Abstract

Fusarium graminearum is the primary causal agent of Fusarium head blight (FHB), a devastating fungal disease on wheat, barley, and other grains. During infection, F. graminearum produces trichothecene mycotoxins, predominately deoxynivalenol (DON), which contaminate grain and reduce grain yield and quality. Although DON functions as a virulence factor to promote F. graminearum spread in the wheat head, it is not essential for establishing initial infection in wheat or barley. When fungal pathogens, such as F. graminearum, infect a host plant, they secrete hundreds of protein effectors that interfere with plant immunity to promote disease. A recent study identified hundreds of putative effector-encoding genes that are conserved across six Fusarium species. In the current study, we selected a subset of 50 conserved effectors from F. graminearum PH-1 and determined their expression on wheat heads over a seven-day infection period. Gene expression analysis revealed that several genes were highly induced in wheat heads during fungal infection. One of them was a putative rhamnogalacturonan acetylesterase homolog (FgRGAE), which was also highly induced in barley heads. FHB virulence assays showed that deletion mutants of FgRGAE significantly reduced initial infection and DON accumulation in wheat and barley heads compared to wild-type controls. Replacing the FgRGAE::Hyg deletion construct with a FgRGAE^ORF+::Gen construct at the native locus restored FHB disease to wild-type levels in both wheat and barley heads. FgRGAE may serve as an ideal target to reduce FHB and mycotoxin contamination in wheat and barley.