Loci controlling resistance to high plains virus and wheat streak mosaic virus in a B73 x Mo17 population of maize

High Plains disease has the potential to cause significant yield loss in su sceptible corn (Zea mays L.) and wheat (Triticum aestivum L.) genotypes, es pecially in the central and western USA. The primary causal agent, High Pla ins virus (HPV), is vectored by wheat curl mite (WCM; Aceria tossichella Ke ifer), which is also the vector of wheat streak mosaic virus (WSMV). In gen eral, the two diseases occur together as a mixed infection in the field. Th e objective of this research was to characterize the inheritance of HPV and WSMV resistance using B73 (resistant to HPV and WSMV) X Mo17 (moderately s usceptible to HPV and WSMV) recombinant inbred lines. A population of 129 r ecombinant inbred lines scored for 167 molecular markers was used to evalua te resistance to WSMV and to a mixed infection of WSMV and HPV. Loci confer ring resistance to systemic movement of WSMV in plants mapped to chromosome s 3, 6, and 10, consistent with the map position of wsm2, wsm1, and wsm3, r espectively. Major genes for resistance to systemic spread of HPV in doubly infected plants mapped to chromosomes 3 and 6, coincident or tightly linke d with the WSMV resistance loci. Analysis of doubly infected plants reveale d that chromosome 6 had a major effect on HPV resistance, consistent with o ur previous analysis of B73 X W64A and B73 x Wf9 populations. Quantitative trait loci (QTL) affecting resistance to localized symptom development mapp ed to chromosomes 4 (umc66), 5 (bn15.40), 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. Id entification of cosegregating markers may facilitate selection for HPV and WSMV resistance in corn breeding programs.