Genes for resistance to northern corn leaf blight in diverse maize populations

Turcicum or northern corn leaf blight (NCLB) incited by the ascomycete Seto sphaeria turcica, anamorph Exserohilum turcicum, is a ubiquitous foliar dis ease of maize. Diverse sources of qualitative and quantitative resistance a re available but qualitative resistances (Ht genes) are often unstable. In the tropics especially, they are either overcome by new Virulent races or t hey suffer from climatically sensitive expression. Quantitative resistance is expressed independently of the physical environment and has never succum bed to S. turcica pathotypes in the field. This review emphasizes the ident ification and mapping of genes related to quantitative NCLB resistance. We deal with the consistency of the genomic positions of quantitative trait lo ci (QTL) controlling resistance across different maize populations, and wit h the clustering of genes for resistance to S. turcica and other fungal pat hogens or insect peals in the maize genome. Implications from these finding s for further genomic research and resistance breeding are drawn. Incubation period (IP) and area under the disease progress curve (AUDPC), b ased on multiple disease ratings, are important component traits of quantit ative NCLB resistance. They are generally tightly correlated (r(p) approxim ate to 0.8) and highly heritable (h(2) approximate to 0.75). QTL for resist ance to NCLB (IP and AUDPC) were identified and characterized in three mapp ing populations (A, B, C). population A, a set of 121-150 F-3 families of t he cross B52 x Mo17, represented US Corn Belt germplasm with a moderate lev el of resistance. It was field-tested in Iowa, USA, and Kenya, and genotype d at 112 restriction fragment length polymorphism (RFLP) loci. Population B consisted of 194-256 F, families of the cross Lo951 x CML202, the first pa rent being a Corn-Belt-derived European inbred line and the second parent b eing a highly resistant tropical African inbred line. The population was al so tested in Kenya and genotyped with 110 RFLP markers. Population C was de rived from a cross between two early-maturing European inbred lines, D32 an d D145, both having a moderate level of resistance. A total of 220 F-3 fami lies were tested in Switzerland and characterized with 87 RFLP and seven SS R markers. In each of the three studies, 12-13 QTL were detected by composi te interval mapping at a significance threshold of LOD = 2.5. The phenotypi c and the gene typic variance were explained to an extent of 50-70% and 60- 80%, respectively. Gene action was additive to partly dominant, as in previ ous generation means and combining ability analyses with other genetic mate rial. 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 5.04), and 8 (bin 8.05/06). The major genes Ht2 and Htn1 were also mapped to bins 8.05 and 8.06, sugge sting the presence of a cluster of closely linked major and minor genes. Th e 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 d iseases and insect pests of maize. Bins 1.05/07 and 9.05 were found to carr y population-specific genes for resistance to S. turcica and other organism s. Several disease lesion mimic mutations; resistance gene analogues and ge nes encoding pathogenesis-related proteins were mapped to regions harbourin g NCLB resistance QTL.