Interval mapping of genes for quantitative resistance of maize to Setosphaeria turcica, cause of northern leaf blight, in a tropical environment

• Published in: Molecular breeding 1996, Vol.2 (2), p.143-156
• Main Authors: Dingerdissen, A.L, Geiger, H.H, Lee, M, Schechert, A, Welz, H.G
• Format: Article
• Language: English
• Subjects: blight; chromosome mapping; chromosomes; disease resistance; gene location; genes; genetic effects; genetic markers; genetic variance; genotype; genotype-environment interaction; heritability; linkage (genetics); linkage groups; loci; quantitative traits; restriction fragment length polymorphism; Setosphaeria turcica; Zea mays
• ISSN: 1380-3743; 1572-9788
• DOI: 10.1007/bf00441429

Quantitative trait loci (QTL) involved in the resistance of maize to Setosphaeria turcica, the causal agent of northern leaf blight, were located by interval mapping analysis of 121 F2: 3 lines derived from a cross between Mo17 (moderately resistant) and B52 (susceptible). A linkage map spanning 112 RFLP loci with 15 cM mean interval length was constructed, based on marker data recorded in a previous study. Field tests with artificial inoculation were conducted at three sites in tropical mid- to high-altitude regions of Kenya, East Africa. Host-plant response was measured in terms of incubation period, disease severity (five scoring dates), and the area under the disease progress curve (AUDPC). Heritability of all traits was high (around 0.75). QTL associated with the incubation period were located on chromosomes 2S and 8L. For disease severity and AUDPC, significant QTL were detected in the putative centromeric region of chromosome 1 and on 2S, 3L, 5S, 6L, 7L, 8L and 9S. On 2S the same marker interval which carried a gene enhancing latent period was also associated with reduced disease severity of juvenile plants. QTL on chromosomes 3L, 5S, 7L and 8L were significant across environments but all other QTL were affected by a large genotype X environment interaction. Partially dominant gene action for resistance as well as for susceptibility was prevailing. Single QTL explained 10 to 38% of the phenotypic variation of the traits. All but the QTL on chromosomes 1, 6 and 9 were contributed by the resistant parent Mo17. On chromosome 8L a QTL mapped to the same region as the major race-specific gene Ht2, supporting the hypothesis that some qualitative and quantitative resistance genes may be allelic.