Dept. of Plant Pathology and Plant-Microbe Biology, Cornell University, Ithaca, NY 14853, USA.
BMC Plant Biol. 2010 Jun 8;10:103. doi: 10.1186/1471-2229-10-103.
Studies 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.
Among 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 qNLB1.06(Tx303) (the Tx303 allele at bin 1.06) reduces the efficiency of fungal penetration, while qNLB1.02(B73) (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; qNLB1.06(Tx303) showed greater effectiveness in the field than in the greenhouse. In addition to NLB resistance, qNLB1.02(B73) was associated with resistance to Stewart's wilt and common rust, while qNLB1.06(Tx303) conferred resistance to Stewart's wilt. The non-specific resistance may be attributed to pleiotropy or linkage.
Our 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.
在一系列病理系统中对宿主-病原体相互作用的研究揭示了植物降低发病效率的多种机制。虽然 R 基因介导的抗性赋予了对病原体入侵的高度有效防御反应，但数量抗性与降低疾病进展的中等水平抗性相关。为了检验特定基因座影响真菌发病过程不同阶段的假设，使用了一组玉米导入系来对调控对北方叶斑病（NLB）病原体新月弯孢菌抗性的数量性状基因座（QTL）进行作图和特征分析。为了更好地理解数量抗性的性质，进一步测试了所鉴定的 QTL 是否符合三个次要假设：（1）疾病 QTL 因宿主发育阶段而异；（2）它们的表现因环境而异；（3）它们决定广谱抗性。
在一组 82 个导入系中，有 7 个系被证实比 B73 更具抗性或敏感性。在 BC4F2 分离群体和先进的导入系中验证了两个 NLB QTL。这些位点被指定为 qNLB1.02 和 qNLB1.06，通过比较导入系与 B73 在针对 NLB 发育不同阶段的一系列宏观和微观疾病成分，对这些位点进行了详细研究。温室和田间重复试验表明，qNLB1.06(Tx303)（1.06 -bin 的 Tx303 等位基因）降低了真菌穿透的效率，而 qNLB1.02(B73)（1.02-bin 的 B73 等位基因）增强了围绕感染部位的几丁质和酚类物质的积累，减少了菌丝在维管束中的生长，并损害了叶片中的随后的坏死性定殖。该 QTL 在幼龄和成年植株中同样有效；qNLB1.06(Tx303)在田间的效果优于温室。除了 NLB 抗性外，qNLB1.02(B73)还与斯图尔特氏萎蔫病和普通锈病抗性有关，而 qNLB1.06(Tx303)赋予了斯图尔特氏萎蔫病抗性。非特异性抗性可能归因于多效性或连锁。
我们的研究成功鉴定了两个可靠表达的 QTL，它们有可能在不同环境下被用来保护玉米免受新月弯孢菌的侵害。这种鉴定和剖析植物数量抗性的方法将促进数量抗性在作物保护中的应用。
