Genetic mapping of maize streak virus resistance from the Mascarene source. I. Resistance in line D211 and stability against different virus clones

Maize streak virus (MSV) disease may cause significant grain yield reductio ns in maize in Africa. Reunion island maize germplasm is a proven source of strong resistance. Its genetic control was investigated using 123 RFLP mar kers in an F-2 population of D211 (resistant)x B73 (susceptible). This popu lation of 165 F-2:3 families was carefully evaluated in Harare (Zimbabwe) a nd in Reunion. Artificial infestation was done with viruliferous leafhopper s. Each plant was rated weekly six times after infestation on a 1-9 scale p reviously adjusted by image analysis. QTL analyses were conducted for each scoring date, and for the areas under the disease, incidence and severity p rogress curves. The composite interval mapping method used allowed the esti mation of the additive and dominance effects and QTL x environment interact ions. Heritabilities ranged from 73% to 98%, increasing with time after inf estation. Resistance to streak virus in D211 was provided by one region on chromosome 1, with a major effect, and four other regions on chromosomes 2, 3 (two regions) and 10, with moderate or minor effects. Overall, they expl ained 48-62% of the phenotypic variation for the different variables. On ch romosome 3, one of the two regions seemed to be more involved in early resi stance, whereas the second was detected at the latest scoring date. Other Q TLs were found to be stable over time and across environments. Mild QTL x e nvironment interactions were detected. Global gene action appeared to be pa rtially dominant, in favor of resistance, except at the earliest scoring da tes, where it was additive. From this population, 32 families were chosen, representing the whole range of susceptibility to MSV. They were tested in Reunion against three MSV clones, along with a co-inoculation of two of the m. Virulence differences between clones were significant. There were genoty pe x clone interactions, and these were more marked for disease incidence t han for severity. Although these interactions were not significant for the mean disease scores, it is suggested that breeders should select for comple tely resistant genotypes.