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Genetic variability and mapping of genes controlling resistance to high plains virus (HPV) in maize
Abstract
High Plains disease complex can cause significant yield loss in susceptible maize (Zea mays, L.) and wheat (Triticum aestivum L.em.Thell) genotypes. The primary causal agent, High Plains Virus (HPV) is vectored by wheat curl mite, Aceria tossichella Keifer which is also the vector of wheat streak mosaic virus (WSMV). In general, the two diseases seem to occur together as a mixed infection in the field. Genetic variability for resistance to the HPV was characterized on maize inbred lines to the mixed infection and to WSMV alone based on symptom expression and virus titer measured by ELISA. HPV resistant inbreds include B73 and susceptibles include W64A, Wf9, and N194. In general, inbreds most severely affected by HPV also had a high WSMV titer although they displayed few symptoms when inoculated with WSMV alone. Inheritance of resistance to systemic spread of HPV and WSMV in mixed infection was characterized using crosses B73 x Wf9 and B73 x W64A. Parental, F$\sb1,$ and F$\sb2$ plants were mite-inoculated with HPV and WSMV, and scored for their reactions visually and by ELISA. F$\sb1$ plants indicated that resistance is dominant, and F$\sb2$ generation fit a 3:1 R:S ratio consistent with a single chromosome region segregating for resistance to both viruses. B73 resistant allele was linked to marker bnl6.29 on the short arm of chromosome 6, a region controlling resistance to WSMV. B73 x Mo17 recombinant inbred lines scored for 167 molecular markers were also used to evaluate disease resistance. Loci conferring resistance to systemic movement of WSMV mapped to chromosomes 3, 6, and 10 consistent with the map position of wsm genes. Major genes for resistance to systemic spread of HPV and WSMV in doubly infected plants mapped to chromosome 3 and 6, coincident or tightly linked with the WSMV resistance loci. Chromosome 6 had a major effect on HPV resistance, consistent with analysis of B73 x W64A and B73 x Wf9. QTLs affecting resistance to localized symptom development mapped to chromosomes 4, 5, and 6. Results from this research will provide important new information on the genetic basis of HPV resistance, information which should enhance breeding efforts for resistance to HPV and WSMV infection.
Subject Area
Plant pathology|Genetics|Molecular biology
Recommended Citation
Marcon, Alberto, "Genetic variability and mapping of genes controlling resistance to high plains virus (HPV) in maize" (1997). ETD collection for University of Nebraska-Lincoln. AAI9805515.
https://digitalcommons.unl.edu/dissertations/AAI9805515