GWAS for maize Fusarium ear rot resistance identifies canonical and non-canonical pathogenesis-related genes

Fusarium ear rot (FER), caused by Fusarium verticillioides, lowers grain quality and market value and contaminates kernels with carcinogenic fumonisins. Chemical and cultural controls are inconsistent, and genetic resistance is complex and environment dependent. We integrated multi-environment field phenotyping (2020–2021), genome-wide association studies (mixed models on whole-genome variants), and microbiome-aware heritability modeling in a panel of 272 diverse maize inbreds evaluated under natural infection (NI) and artificial inoculation. The composite FER index aligned most strongly with NI, indicating related but distinct resistance components under the two pressures. GWAS detected 28 significant SNPs across 14 loci on chromosomes 1, 2, 3, 6, 9, and 10. Canonical candidates included an RPM1-interacting protein (RIN-family; RIN13), an AP2/ERF transcription factor, a cytochrome P450, and Villin-4, implicating immune signaling, hormone-mediated defense, detoxification, and cytoskeletal remodeling. Non-canonical, defense-linked candidates PFK1, sucrose-phosphate synthase–like (SPS), malic enzyme 15, a vitamin B6 enzyme, triacylglycerol lipase 1, SNF1-related kinase (KIN11-like), a P4-type phospholipid-transporting ATPase, YSL6 metal–nicotianamine transporter, and an ornithine cyclodeaminase/μ-crystallin–family gene highlight roles for energy/carbon metabolism, redox buffering, membrane-lipid homeostasis, and micronutrient transport. At the association level, most signals are shared by FER and NI, with fewer unique to inoculation, supporting a two-step breeding approach: screen under inoculation to remove highly susceptible lines, then select under NI (or the NI-aligned composite) for durable, field-relevant resistance.