Genes for resistance to northern corn leaf blight in diverse maize populations
Authors: WELZ H. G. , GEIGER H. H. 
Published: March 2003

AbstractTurcicum or northern corn leaf blight (NCLB) incited by the ascomycete Setosphaeria turcica, anamorph Exserohilum turcicum, is a ubiquitous foliar disease of maize. Diverse sources of qualitative and quantitative resistance are available but qualitative resistances (Ht genes) are often unstable. In the tropics especially, they are either overcome by new virulent races or they suffer from climatically sensitive expression. Quantitative resistance is expressed independently of the physical environment and has never succumbed to S. turcica pathotypes in the field. This review emphasizes the identification and mapping of genes related to quantitative NCLB resistance. We deal with the consistency of the genomic positions of quantitative trait loci (QTL) controlling resistance across different maize populations, and with the clustering of genes for resistance to S. turcica and other fungal pathogens or insect pests in the maize genome. Implications from these findings for further genomic research and resistance breeding are drawn.Incubation period (IP) and area under the disease progress curve (AUDPC), based on multiple disease ratings, are important component traits of quantitative NCLB resistance. They are generally tightly correlated (rp≅ 0.8) and highly heritable (h2≅ 0.75). QTL for resistance to NCLB (IP and AUDPC) were identified and characterized in three mapping populations (A, B, C). Population A, a set of 121‐150 F3 families of the cross B52×mo17, represented US Corn Belt germplasm with a moderate level of resistance. It was field‐tested in Iowa, USA, and Kenya, and genotyped at 112 restriction fragment length polymorphism (RFLP) loci. Population B consisted of 194‐256 F3 families of the cross Lo951×CML202, the first parent being a Corn‐Belt‐derived European inbred line and the second parent being a highly resistant tropical African inbred line. The population was also tested in Kenya and genotyped with 110 RFLP markers. Population C was derived from a cross between two early‐maturing European inbred lines, D32 and D145, both having a moderate level of resistance. A total of 220 F3 families were tested in Switzerland and characterized with 87 RFLP and seven SSR markers. In each of the three studies, 12‐13 QTL were detected by composite interval mapping at a signifcance threshold of LOD=2.5. The phenotypic and the genotypic variance were explained to an extent of 50‐70% and 60‐80%, respectively. Gene action was additive to partly dominant, as in previous generation means and combining ability analyses with other genetic material. In each population, gene effects of the QTL were of similar magnitude and no putative major genes were discovered. QTL for AUDPC were located on chromosomes 1 to 9. All three populations carried QTL in identical genomic regions on chromosomes 3 (bin 3.06/07), 5 (bin 3.06/07) and 8 (bin 8.05/06). The major genes Ht2 and Htn1 were also mapped to bins 8.05 and 8.06, suggesting the presence of a cluster of closely linked major and minor genes. The chromosomal bins 3.05, 5.04 and 8.05, or adjacent intervals, were further associated with QTL and major genes for resistance to eight other fungal diseases and insect pests of maize. Bins 1.05/07 and 9.05 were found to carry population‐specifc genes for resistance to S. turcica and other organisms. Several disease lesion mimic mutations, resistance gene analogues and genes encoding pathogenesis‐related proteins were mapped to regions harbouring NCLB resistance QTL.