RESISTANCE TO SYSTEMIC SPREAD OF HIGH-PLAINS VIRUS AND WHEAT STREAK MOSAIC-VIRUS COSEGREGATES IN 2 F-2 MAIZE POPULATIONS INOCULATED WITH BOTH PATHOGENS

High plains virus (HPV) has the potential to cause significant damage in susceptible maize (Zea mays L.) genotypes. The virus is vectored by the wheat curl mite (WCM), Aceria tosichella, Keifer, which also vect ors wheat streak mosaic virus (WSMV). We have previously characterized susceptibility of maize inbred lines to double infection of HPV slid WSMV. The objective of this study was to characterize the inheritance of resistance to systemic spread of HPV and WSMV in mixed infection. G enetic analysis was done with crosses B73 (resistant) x Wf9 (susceptib le) and B73 x W64A (susceptible). Parental, F-1, and F-2 plants were W CM-inoculated with HPV and WSMV, and scored for their reactions both v isually and by enzyme-linked immunosorbent assay. F-1 plants were resi stant to systemic spread of HPV and WSMV, indicating that resistance i s dominant in these lines. Segregation (based on symptomology) in the F-2 generation fit a 3:1 resistant:susceptible ratio in both B73 x W64 A and B73 x Wf9 (P = 0.34 and 0.11, respectively), consistent with a s ingle chromosome region segregating for resistance to both viruses. Th e resistant allele was contributed by B73 and was Linked to marker bnl 6.29 on the short arm of chromosome six. This chromosome region has be en shown to control resistance to WSMV (wsm1). Two independent sets of inbred-backcross-derived near-isogenic lines confirmed the effect of this chromosome region. This study reveals the genetic basis of sympto mology observed upon mixed infection with HPV and WSMV in these popula tions. Identification of molecular markers linked to virus resistance genes may enhance inbred line development efforts.