Date of this Version
Crop Sci. 39:1171-1177 (1999).
High Plains disease has the potential to cause significant yield loss in susceptible corn (Zea mays L.) and wheat (Triticum aestivum L.) genotypes, especially in the central and western USA. The primary causal agent, High Plains virus (HPV), is vectored by wheat curl mite (WCM; Aceria tossicheila Keifer), which is also the vector of wheat streak mosaic virus (WSMV). In general, the two diseases occur together as a mixed infection in the field. The objective of this research was to characterize the inheritance of HPV and WSMV resistance using B73 (resistant to HPV and WSMV) × Mo17 (moderately susceptible to HPV and WSMV) recombinant inbred lines. A population of 129 recombinant inbred lines scored for 167 molecular markers was used to evaluate resistance to WSMV and to a mixed infection of WSMV and HPV. Loci conferring resistance to systemic movement of WSMV in plants mapped to chromosomes 3, 6, and 10, consistent with the map position of wsm2, wsm1, and wsm3, respectively. Major genes for resistance to systemic spread of HPV in doubly infected plants mapped to chromosomes 3 and 6, coincident or tightly linked with the WSMV resistance loci. Analysis of doubly infected plants revealed that chromosome 6 had a major effect on HPV resistance, consistent with our previous analysis of B73 × W64A and B73 × Wf9 populations. Quantitative trait loci (QTL) affecting resistance to localized symptom development mapped to chromosomes 4 (umc66), 5 (bnl5.40), and 6 (umc85), and accounted for 24% of the phenotypic variation. Localized symptoms may reflect the amount of mite feeding or the extent of virus spread at the point of infection. Identification of cosegregating markers may facilitate selection for HPV and WSMV resistance in corn breeding programs.