Dissection of Common Rust Resistance in Tropical Maize Multiparent Population through GWAS and Linkage Studies

Abstract

Common rust (CR), caused by Puccina sorghi, is a major foliar disease in maize that leads to quality deterioration and yield losses. To dissect the genetic architecture of CR resistance in maize, this study utilized the susceptible temperate inbred line Ye107 as the male parent crossed with three resistant tropical maize inbred lines (CML312, D39, and Y32) to generate 627 F7 recombinant inbred lines (RILs), with the aim of identifying maize disease-resistant loci and candidate genes for common rust. Phenotypic data showed good segregation between resistance and susceptibility, with varying degrees of resistance observed across different subpopulations. Significant genotype effects and genotype × environment interactions were observed, with heritability ranging from 85.7% to 92.2%. Linkage and genome-wide association analyses across the three environments identified 20 QTLs and 62 significant SNPs. Among these, seven major QTLs explained 66% of the phenotypic variance. Comparison with six SNPs repeatedly identified across different environments revealed overlap between qRUST3-3 and Snp-203,116,453, and Snp-204,202,469. Haplotype analysis indicated two different haplotypes for CR resistance for both the SNPs. Based on LD decay plots, three co-located candidate genes, Zm00001d043536, Zm00001d043566, and Zm00001d043569, were identified within 20 kb upstream and downstream of these two SNPs. Zm00001d043536 regulates hormone regulation, Zm00001d043566 controls stomatal opening and closure, related to trichome, and Zm00001d043569 is associated with plant disease immune responses. Additionally, we performed candidate gene screening for five additional SNPs that were repeatedly detected across different environments, resulting in the identification of five candidate genes. These findings contribute to the development of genetic resources for common rust resistance in maize breeding programs.