Data from: Genetic analysis of sugarcane mosaic virus resistance in the Wisconsin Diversity Panel of maize

Sugarcane mosaic virus (SCMV) and Maize dwarf mosaic virus can cause yield loss in maize (Zea mays L.). Previous studies identified two key genomic regions controlling host resistance: Scmv1 on chromosome 6 and Scmv2 on chromosome 3. In this study a diverse set of 578 inbreds adapted to a northern US Corn Belt environment, was inoculated at the three-leaf stage with SCMV and rated for presence of virus symptoms at 7, 10, 14, 21, 28, and 35 d after inoculation. Scmv1 was present in all resistant inbreds. A single-nucleotide polymorphism associated with SCMV resistance was found 5 Mb downstream of the putative location of Scmv1, and resistance at this downstream locus was correlated with a group of inbreds containing the presence allele of a 2.7-Mb presence–absence variation (PAV) in the region encompassing Scmv1. The Scmv2 region was associated with resistance 35 d after inoculation only among the inbreds containing the presence allele, including Scmv1. Several other loci unlinked to Scmv1 and Scmv2 were associated with resistance in this panel, providing evidence for multigenic modification of the efficacy of Scmv1 and Scmv2. Sixty-nine inbreds representing haplotype variation in the region surrounding Scmv1 on chromosome 6 were inoculated with SCMV at the three- and six-leaf stage. Symptom development was reduced when inoculation was delayed to the six-leaf stage, but 24 inbreds became fully symptomatic after 35 d regardless of the growth stage at inoculation. Inbreds with the presence allele of the PAV encompassing Scmv1 were more resistant to SCMV when inoculation was delayed to the six-leaf stage than those that had the absence allele. Inbreds with the absence allele were susceptible regardless of growth stage at inoculation.甘蔗花叶病毒（Sugarcane mosaic virus, SCMV）与玉米矮花叶病毒均可造成玉米（Zea mays L.）产量损失。既往研究已鉴定出两个调控寄主抗性的关键基因组区域：位于6号染色体的Scmv1，以及位于3号染色体的Scmv2。本研究以578份适配美国北部玉米带种植环境的多样化自交系为材料，于三叶期接种SCMV，并分别于接种后7、10、14、21、28及35 d评估病毒症状的发生情况。所有抗性自交系均携带Scmv1区域。研究人员在推定的Scmv1位点下游5 Mb处，发现了与SCMV抗性相关的单核苷酸多态性（single-nucleotide polymorphism）；该下游位点的抗性表型，与携带Scmv1区域内2.7 Mb存在-缺失变异（presence–absence variation, PAV）存在等位基因的一类自交系显著相关。Scmv2区域仅在携带该存在等位基因（含Scmv1）的自交系中，与接种后35 d的抗性表现相关。本研究群体中还鉴定出多个与Scmv1、Scmv2无遗传连锁关系的抗性相关位点，提示Scmv1与Scmv2的抗病效应可通过多基因修饰进行调控。此外，研究人员选取69份代表6号染色体Scmv1区域单倍型变异的自交系，分别于三叶期和六叶期接种SCMV。结果显示，将接种时间延迟至六叶期可减轻症状发展，但仍有24份自交系无论接种时的生育期如何，均在接种后35 d出现完全显症。携带Scmv1区域PAV存在等位基因的自交系，在延迟至六叶期接种时的抗病性显著高于携带缺失等位基因的材料；而携带缺失等位基因的自交系无论接种生育期如何，均表现为感病。