Identifying candidate genes associated with resistance to northern leaf blight (NLB) will greatly enhance maize breeding programs aiming at reducing maize grain yield losses caused by NLB. In this study, a multi-parental population (MPP) was constructed consisting of four recombined inbred line (RIL) subpopulations, all sharing a common parent Ye107, for GWAS and linkage analysis. The results revealed the detection of a significant SNP, 5-49193921, from a tropical maize inbred line YML226. This SNP was found to be associated with the gene Zm00001d014471, which encodes a pentatricopeptide repeat (PPR-like) superfamily protein. Furthermore, gene expression analysis showed a positive correlation between the expression of Zm00001d014471 and NLB resistance. Notably, the F 1 generation of YML226 × Ye107 contained the largest number of specific SNPs within the genic region, suggesting that its abundant genetic variation might contribute to its high NLB resistance. Furthermore, there was a specific nonsynonymous SNP (C to T) causing a nucleotide change at position 235, leading to an alteration of an amino acid, which resulted in the modification of a motif in the PPR protein. Our results revealed that tropical maize germplasm YML226 could serve an important genetic resource for NLB resistance. Additionally, previous studies have shown that YML226 is an exceptional elite line derived from CATETO germplasm, exhibiting a higher positive general combining ability for grain yield. Therefore, YML226 holds great promise for the breeding of NLB-resistant maize cultivars in the future.

Plants adaptively change their cell wall composition and structure during growth, development, and interactions with environmental stresses. Dirigent proteins (DIRs) contribute to environmental adaptations by dynamically reorganizing the cell wall and/or by generating defense compounds. We established that maize DIR ZmDRR206 (DISEASE RESISTANCE RESPONSE206) mediates maize seedling growth and disease resistance response by coordinately regulating biosynthesis of cell wall components for cell wall integrity (CWI) maintenance. ZmDRR206 responded to pathogen infection by rapidly increasing its expression. Both mutation and overexpression of ZmDRR206 resulted in similar small kernel and diminished seedling growth; while ZmDRR206-overexpression increased disease resistance, greater drought tolerance and reduced photosynthetic activity, thus caused maize seedlings to show a growth-defense trade-off phenotype. Consistently, ZmDRR206-overexpression reduced the contents of primary metabolites and down-regulated the photosynthesis-related genes; while increased the contents of major cell wall components and defense phytohormones; up-regulated defense- and cell wall biosynthesis-related genes in maize seedlings grown under non-stress conditions. Furthermore, ZmDRR206 physically interacted with ZmCesA10, a secondary cell wall-specific cellulose synthase catalytic subunit, in yeast and in planta. Our findings unravel a mechanism that ZmDRR206 maintains CWI during maize seedling growth, providing opportunities for breeding strong disease resistance in maize.