<i>Fusarium verticillioides</i> Induces Maize-Derived Ethylene to Promote Virulence by Engaging Fungal G-Protein Signaling

Abstract

Seed maceration and contamination with mycotoxin fumonisin inflicted by <i>Fusarium verticillioides</i> is a major disease concern for maize producers worldwide. Meta-analyses of quantitative trait loci for Fusarium ear rot resistance uncovered several ethylene (ET) biosynthesis and signaling genes within them, implicating ET in maize interactions with <i>F. verticillioides</i>. We tested this hypothesis using maize knockout mutants of the 1-aminocyclopropane-1-carboxylate (ACC) synthases <i>ZmACS2</i> and <i>ZmACS6</i>. Infected wild-type seed emitted five-fold higher ET levels compared with controls, whereas ET was abolished in the <i>acs2</i> and <i>acs6</i> single and double mutants. The mutants supported reduced fungal biomass, conidia, and fumonisin content. Normal susceptibility was restored in the <i>acs6</i> mutant with exogenous treatment of ET precursor ACC. Subsequently, we showed that fungal G-protein signaling is required for virulence via induction of maize-produced ET. <i>F. verticillioides</i> G_β subunit and two regulators of G-protein signaling mutants displayed reduced seed colonization and decreased ET levels. These defects were rescued by exogenous application of ACC. We concluded that pathogen-induced ET facilitates <i>F. verticillioides</i> colonization of seed, and, in turn, host ET production is manipulated via G-protein signaling of <i>F. verticillioides</i> to facilitate pathogenesis.[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.