Data from: Genetic analysis of sugarcane mosaic virus resistance in the Wisconsin Diversity Panel of maize
Cite this dataset
Gustafson, Timothy J.; de Leon, Natalia; Kaeppler, Shawn M.; Tracy, William F. (2019). Data from: Genetic analysis of sugarcane mosaic virus resistance in the Wisconsin Diversity Panel of maize [Dataset]. Dryad. https://doi.org/10.5061/dryad.dq91858
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.