BackgroundStudies on host-pathogen interactions in a range of pathosystems have revealed an array of mechanisms by which plants reduce the efficiency of pathogenesis. While R-gene mediated resistance confers highly effective defense responses against pathogen invasion, quantitative resistance is associated with intermediate levels of resistance that reduces disease progress. To test the hypothesis that specific loci affect distinct stages of fungal pathogenesis, a set of maize introgression lines was used for mapping and characterization of quantitative trait loci (QTL) conditioning resistance to Setosphaeria turcica, the causal agent of northern leaf blight (NLB). To better understand the nature of quantitative resistance, the identified QTL were further tested for three secondary hypotheses: (1) that disease QTL differ by host developmental stage; (2) that their performance changes across environments; and (3) that they condition broad-spectrum resistance.ResultsAmong a set of 82 introgression lines, seven lines were confirmed as more resistant or susceptible than B73. Two NLB QTL were validated in BC4F2 segregating populations and advanced introgression lines. These loci, designated qNLB1.02 and qNLB1.06, were investigated in detail by comparing the introgression lines with B73 for a series of macroscopic and microscopic disease components targeting different stages of NLB development. Repeated greenhouse and field trials revealed that qNLB1.06Tx303 (the Tx303 allele at bin 1.06) reduces the efficiency of fungal penetration, while qNLB1.02B73 (the B73 allele at bin 1.02) enhances the accumulation of callose and phenolics surrounding infection sites, reduces hyphal growth into the vascular bundle and impairs the subsequent necrotrophic colonization in the leaves. The QTL were equally effective in both juvenile and adult plants; qNLB1.06Tx303 showed greater effectiveness in the field than in the greenhouse. In addition to NLB resistance, qNLB1.02B73 was associated with resistance to Stewart's wilt and common rust, while qNLB1.06Tx303 conferred resistance to Stewart's wilt. The non-specific resistance may be attributed to pleiotropy or linkage.ConclusionsOur research has led to successful identification of two reliably-expressed QTL that can potentially be utilized to protect maize from S. turcica in different environments. This approach to identifying and dissecting quantitative resistance in plants will facilitate the application of quantitative resistance in crop protection.

As part of a larger effort to capture diverse alleles at a set of loci associated with disease resistance in maize, DK888, a hybrid known to possess resistance to multiple diseases, was used as a donor in constructing near-isogenic lines (NILs). A NIL pair contrasting for resistance to northern leaf blight (NLB), caused by Setosphaeria turcica, was identified and associated with bin 8.06. This region of the maize genome had been associated in previous studies with both qualitative and quantitative resistance to NLB. In addition, bins 8.05-8.06 had been associated with quantitative resistance to several other diseases, as well as resistance gene analogs and defense response gene homologs. To test the hypothesis that the DK888 allele at bin 8.06 (designated qNLB8.06 ( DK888 )) conditions the broad-spectrum quantitative resistance characteristic of the donor, the NILs were evaluated with a range of maize pathogens and different races of S. turcica. The results revealed that qNLB8.06 (DK888) confers race-specific resistance exclusively to NLB. Allelism analysis suggested that qNLB8.06 (DK888) is identical, allelic, or closely linked and functionally related to Ht2. The resistance conditioned by qNLB8.06 was incompletely dominant and varied in effectiveness depending upon allele and/or genetic background. High-resolution breakpoint analysis, using approximately 2,800 individuals in F(9)/F(10) heterogeneous inbred families and 98 F(10)/F(11) fixed lines carrying various recombinant events, delimited qNLB8.06 ( DK888 ) to a region of approximately 0.46 Mb, spanning 143.92-144.38 Mb on the B73 physical map. Three compelling candidate genes were identified in this region. Isolation of the gene(s) will contribute to better understanding of this complex locus.