Diverse modes of gene action contribute to heterosis for quantitative disease resistance in maize.

This article focuses on the genetic architecture and heterosis (hybrid vigor) of quantitative disease resistance in maize against two foliar fungal diseases: southern leaf blight (SLB) caused by *Cochliobolus heterostrophus* and gray leaf spot (GLS) caused by *Cercospora zeae-maydis*. Using the Intermated B73 by Mo17 (IBM) recombinant inbred line (RIL) population and reciprocal backcrosses, the study identified multiple quantitative trait loci (QTL) exhibiting diverse modes of gene action—including additive, dominance, overdominance, and epistasis—that contribute to resistance and heterosis. The findings reveal that heterosis for disease resistance varies depending on the specific hybrid genotype and disease, with both dominant resistance and dominant susceptibility alleles playing significant roles, contrasting with the typical dominance of resistance alleles in qualitative resistance. Additionally, epistatic interactions between QTL were detected, further complicating the inheritance patterns of quantitative resistance. This research provides detailed insights into the complex genetic basis of quantitative disease resistance and its contribution to heterosis in maize.