Quantitative and qualitative trait loci affecting host-plant response to Exserohilum turcicum in maize (Zea mays L.)

Abstract

Molecular markers at 103 loci were used to identify the location of quantitative sources of resistance to Exserohilum turcicum in 150 F2∶3 lines of a B52/Mo17 maize population. Host-plant response was measured in terms of the average number of lesions per leaf, the average percent leaf tissue diseased (severity), and the average size of lesions. The location of quantitative trait loci were compared with three loci having known qualitative effects, namely Ht1, Ht2 and bx1. Chromosomal regions containing the Ht1 and Ht2 loci showed a small contribution in determining lesion size, even though alleles with dominant, qualitative effects at these loci have never been reported in either inbred parent. Similar effects were not observed for the number of lesions or for disease severity. Likewise, some contribution was observed for chromosomal regions encompassing the bx1 locus in determining lesion size but not the number of lesions or disease severity. Overall the contribution of loci in the vicinity of Ht1, Ht2 and bx1 was small relative to variation attributable to loci with quantitative effects identified in this study. Molecular-marker-facilitated mapping concurred with previous reciprocal translocation mapping studies on the importance of chromosomes 3, 5 and 7, despite the fact that these studies utilized diverse sources of resistant germplasm.

Precise Mapping of Quantitative Trait Loci for Resistance to Southern Leaf Blight, Caused by Cochliobolus heterostrophus Race O, and Flowering Time Using Advanced Intercross Maize Lines

“…There are many examples of reports identifying QTL effective under varying levels of a particular stress (e.g., LeDeaux et al 2006;Vargas et al 2006), but, to our knowledge, this is the first report directly comparing disease-resistance QTL identified under varying levels of disease pressure in the absence of other variables. Disease-resistance QTL for northern leaf blight of maize were detected at fairly consistent positions within the same population evaluated in differing environments in Iowa and Kenya (Freymark et al 1993(Freymark et al , 1994Dingerdissen et al 1996). Disease pressure was more severe in Kenya than in Iowa, implying that similar resistance mechanisms were effective under variable disease pressure also for northern leaf blight.…”

Unraveling Genomic Complexity at a Quantitative Disease Resistance Locus in Maize

“…In a QTL study of the recombinant inbred line (RIL) population Ki14 3 B73 evaluated for three foliar fungal diseases, NLB, GLS, and SLB, a 33-Mb region spanning bins 1.05 and 1.06 was the only locus identified that conferred resistance to all three diseases (Zwonitzer et al 2010). A number of QTL studies for NLB resistance in maize have identified QTL at bin 1.06, ranging in physical size from 3 to 30 Mb (Freymark et al 1993;Welz et al 1999;Wisser et al 2006;Chung et al 2010bChung et al , 2011Van Esbroeck et al 2010;Poland et al 2011). Additionally, bin 1.06 harbors the dominant Stewart's wilt resistance gene Sw1 (Ming et al 1999).…”

Use of IPM in the control of multiple diseases in maize: Strategies for selection of host resistance

“…Several groups mapped QTL responsible for quantitative resistance to E. turcicum (Welz et al, 1998;Freymark et al, 1993;Schechert et al, 1999;Dingerdissen et al, 1996). The consistency of results among these studies was intermediate between the MSV and GLS studies.…”

“…In addition to the differences in experimental design inherent to all QTL experiments, this may have been due to the fact that both qualitative (major gene) and quantitative (polygene) modes of resistance to E. turcicum have been identified (Raymundo and Hooker, 1982). Freymark et al, (1993) utilized Mo17, an inbred with moderate levels of partial resistance, and B52, a highly susceptible inbred, in their mapping study. A population of F 2:3 lines was genotyped and resistance QTL on chromosomes 1, 3, 5, 7 and 8 that were common across two environments were found.…”

“…A population of F 2:3 lines was genotyped and resistance QTL on chromosomes 1, 3, 5, 7 and 8 that were common across two environments were found. Dingerdissen et al (1996) utilized the same Mo17 x B52 population and genetic linkage map developed by Freymark et al (1993) to evaluate E. turcicum resistance in replicated field trials in Kenya. QTL on chromosomes 3, 5, 7 and 8 for disease severity were significant across environments.…”