Nature of resistance of sweetpotato to sweetpotato virus disease
2002
Mwanga, R.O.M. | Moyer, J.W. | Zhang, D.P. | Carey, E.E. | Yencho, G.C.
Sweetpotato virus disease (SPVD) is a disease syndrome due to the dual infection and synergistic interaction of sweetpotato chlorotic stunt crinivirus (SPCSV) and sweetpotato feathery mottle potyvirus (SPFMV). SPVD causes up to 98% yield loss in East Africa. Uganda’s sweetpotato breeding program released six sweetpotato cultivars with moderate to high levels of field SPVD resistance in 1995. A multidisciplinary partnership involving Namulonge Agricultural and Animal Production Research Institute in Uganda, North Carolina State University, the US Vegetable laboratory (USV, USDA-ARS) and Clemson University, Charleston, South Carolina, and the International Potato Center (CIP), Lima, Peru, has investigated the genetic basis of SPVD resistance. This paper highlights research findings of the response of sweetpotato to sweetpotato virus disease. General combining ability (GCA) and specific combining ability of (SCA) of 45 sweetpotato diallel families, and the GCA to SCA variance component ratios were high, indicating that additive gene effects are predominant in the inheritance of SPVD and recovery. The distribution of SPVD scores in the promising families was skewed toward highly susceptible categories in Uganda and Peru. In the proposed model for inheritance, two genes are unlinked and they are inherited in a hexosamic or tetradisomic manner. Based on amplified fragment length polymorphism (AFLP) and quantitative trait loci (QTL) analyses, two unlinked AFLP markers were associated with the loci conferring resistance to SPCSV and SPFMV.
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