An RGAE Homolog in <i>Fusarium graminearum</i> Is Critical for Initial Infection in Wheat and Barley

<i>Fusarium graminearum</i> is the primary causal agent of Fusarium head blight (FHB), a devastating fungal disease on wheat, barley, and other grains. During infection, <i>F. graminearum</i> produces trichothecene mycotoxins, predominately deoxynivalenol (DON), that contaminate grain and reduce grain yield and quality. Although DON functions as a virulence factor to promote <i>F. graminearum</i> spread in the wheat head, it is not essential for establishing initial infection in wheat or barley. When fungal pathogens, such as <i>F. graminearum</i>, 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 <i>Fusarium</i> species. In the current study, we selected a subset of 50 conserved effectors from <i>F. graminearum</i> PH-1 and determined their expression on wheat heads over a 7-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 <u>r</u>hamno<u>g</u>alacturonan <u>a</u>cetyl<u>e</u>sterase homolog (<i>FgRGAE</i>), which was also highly induced in barley heads. FHB virulence assays showed that deletion mutants of <i>FgRGAE</i> significantly reduced initial infection and DON accumulation in wheat and barley heads compared with wild-type controls. Replacing the <i>FgRGAE</i>::<i>Hyg</i> deletion construct with an <i>FgRGAE^ORF+</i>::<i>Gen</i> construct at the native locus restored FHB disease to wild-type levels in both wheat and barley heads. <i>FgRGAE</i> may serve as an ideal target to reduce FHB and mycotoxin contamination in wheat and barley. [Formula: see text] Copyright © 2025 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.