Resistance to Systemic Spread of High Plains Virus and Wheat Streak Mosaic Virus Cosegregates in Two F2 Maize Populations Inoculated with Both Pathogens
- A. Marçon,
- S.M. Kaeppler* and
- S.G. Jensen
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 vectors wheat streak mosaic virus (WSMV). We have previously characterized susceptibility of maize inbred lines to double infection of HPV and WSMV. The objective of this study was to characterize the inheritance of resistance to systemic spread of HPV and WSMV in mixed infection. Genetic analysis was done with crosses B73 (resistant) × Wf9 (susceptible) an B73 × W64A (susceptible). Parental, F1, and F2 plants were WCM-inoculated with HPV and WSMV, and scored for their reactions both visually and by enzymelinked immunosorbent assay. F1 plants were resistant to systemic spread of HPV and WSMV, indicating that resistance is dominant in these lines. Segregation (based on symptomology) in the F2 generation fit a 3:1 resistant:susceptible ratio in both B73 × W64A and B73 × Wf9 (P = 0.34 and 0.11, respectively), consistent with a single chromosome region segregating for resistance to both viruses. The resistant allele was contributed by B73 and was linked to marker bnl6.29 on the short arm of chromosome six. This chromosome region has been 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 symptomology observed upon mixed infection with HPV and WSMV in these populations. Identification of molecular markers linked to virus resistance genes may enhance inbred line development efforts.
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