Insights into the genetic and biochemical basis of Gibberella ear rot resistance in maize

Fusarium graminearum colonizes the maize ear, causing Gibberella ear rot (GER) and producing harmful mycotoxins, including deoxynivalenol (DON) and zearalenone (ZEA). The disease can be managed in part by breeding and planting resistant maize cultivars. Resistance to GER is a quantitative and complex trait. Evaluation of diverse germplasm to identify regions and candidate genes associated with resistance may be useful for crop improvement efforts. Screening for GER is time-consuming and costly. Thus, identifying other traits that may serve as a proxy for GER resistance may accelerate resistance breeding efforts. We hypothesized that grain phenylpropanoid content and kernel composition are genetically and mechanistically related to GER resistance. We screened a diverse set of maize inbred lines for disease severity, DON, ZEA, ferulic acid, p-coumaric acid, pericarp thickness, and several kernel composition traits. Using a genome-wide association study, we identified markers associated with each phenotype and genomic regions that harbor alleles for both disease and metabolite-related phenotypes. Pathways significantly associated with GER-related traits were related to detoxification, cell wall integrity, and lignin biosynthesis. End-season ferulic acid and p-coumaric acid concentrations are not strong proxies for GER resistance, but secondary metabolites are important components of the maize-Fusarium graminearum pathosystem. Furthermore, lignin-deficient brown midrib mutants exhibited increased susceptibility to GER, underscoring the importance of lignin composition in limiting fungal colonization. The study highlights the multifaceted nature of GER resistance, involving both biochemical and structural defenses. These findings provide valuable targets for breeding programs aiming to enhance GER resistance and reduce mycotoxin contamination in maize.