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Abstract
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.
Highlights
Studies on host-pathogen interactions in a range of pathosystems have revealed an array of mechanisms by which plants reduce the efficiency of pathogenesis
Identification of outliers and putative northern leaf blight (NLB) quantitative trait loci (QTL) in the TBBC3 population The full set of 82 TBBC3 lines was screened for NLB resistance at field sites in New York and North Carolina in 2006
In the trial at Aurora New York (NY), three lines were scored as significantly more resistant and 20 lines were scored as significantly more susceptible than B73 for primary diseased leaf area (DLA), while no lines showed significantly more resistance and 39 lines showed more susceptibility than B73 based on area under the disease progress curve (AUDPC)
Summary
Studies on host-pathogen interactions in a range of pathosystems have revealed an array of mechanisms by which plants reduce the efficiency of pathogenesis. A large number of quantitative trait loci (QTL) for disease resistance have been mapped in plants [6,9], but little is known about the underlying genetic basis or defense mechanisms involved. A range of genetic mechanisms controlling basal resistance, defense signalling pathways, detoxification, morphology, and development in the plant host, is hypothesized to be associated with reducing disease progress [6]. Previous QTL studies for foliar diseases have mapped distinct loci associated with incubation period, lesion number, lesion size, or diseased leaf area, with results suggesting that defense genes affecting lesion formation and lesion expansion may not be the same. These observations suggest that distinct resistance mechanisms govern different macroscopic components of resistance
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