Mapping and Genetic Dissection of Novel Tar Spot Resistance QTL on Maize Chromosome 1

Abstract

Abstract Tar spot, caused by the obligate fungus Phyllachora maydis , significantly threatens maize ( Zea mays L.) production across the Americas. Host genetic resistance offers the most viable long-term management strategy. Building on observed differential tar spot tolerance in parents B73 and Mo17, we utilized a strategic core subset of 94 intermated B73 × Mo17 (IBM-94) population to characterize the genetic architecture of resistance. Phenotypic analysis of a panel of 96 recombinant inbreds including the susceptible parent, Mo17, and the moderately resistant parent, B73 confirmed stable differences in susceptibility, with B73 consistently demonstrating moderate resistance compared to Mo17. Analysis of variance revealed highly significant genetic variation within the population (F = 12.96; p < 0.001). High Pearson correlation (r = 0.8706, p < 0.0001) and coefficient of determination (R 2 = 0.7579) across environments indicated that 76% of the phenotypic variance is attributable to genetic factors. Linkage mapping identified a novel, consistent major QTL cluster on chromosome 1. This cluster comprises five regions (qTAR_1.1 through qTAR_1.5) exceeding the significance threshold (LOD 3.8) in both years. We identified 74 candidate genes including bZIP, and RING/U-box proteins at significant SNP peaks. Additionally, gene annotation revealed a high concentration of wall-associated kinases and S-locus lectin protein kinases within the qTAR_1.4 and qTAR_1.5 regions, alongside potential defense-related transcription factors (MYB, bZIP, and C2H2 zinc fingers).These findings provide a framework for high-resolution mapping and functional validation to accelerate the development of tar spot-resistant maize cultivars.