Molecular markers linked to resistance to sweetpotato chlorotic stunt closterovirus [SPCSV (genus Crinivirus, family Closteroviridae)] and sweetpotato feathery mottle virus [SPFMV (genus Potyvirus, family Potyviridae)] were selected using quantitative trait loci (QTL) analysis, discriminant analysis and logistic regression. Eighty-seven F1 sweetpotato [Ipomoea batatas (L.) Lam.] genotypes from a cross of `Tanzania' and `Wagabolige' landraces were used to generate DNA marker profiles for this study. Forty-five of the clones were resistant to SPCSV while 37 were resistant to SPFMV. A combination of 232 amplified fragment length polymorphism (AFLP) markers and 37 random amplified polymorphic DNA (RAPD) markers obtained were analyzed to determine the most informative markers. All three statistical procedures revealed that AFLP marker e41m33.a contributed the greatest variation in SPCSV resistance and RAPD marker S13.1130 accounted for most of the variation in SPFMV resistance. The power of discriminant and logistic analyses is that you do not need a parent-progeny population. An evaluation of these two models indicated a classification and prediction accuracy rates of 96% with as few as four markers in a model. Both multivariate techniques identified one important discriminatory marker (e44m41.j) for SPCSV and two markers (e41m37.a and e44m36.d) for SPFMV that were not identified by QTL analysis.
When sweetpotato chlorotic stunt crinivirus (SPCSV) and sweetpotato feathery mottle potyvirus (SPFMV) infect sweetpotato [Ipomoea batatas (L.) Lam.], they interact synergistically and cause sweetpotato virus disease (SPVD), a major constraint to food productivity in east Africa. The genetic basis of resistance to these diseases was investigated in 15 sweetpotato diallel families (1352 genotypes) in Uganda, and in two families of the same diallel at the International Potato Center (CIP), Lima, Peru. Graft inoculation with SPCSV and SPFMV resulted in severe SPVD symptoms in all the families in Uganda. The distribution of SPVD scores was skewed toward highly susceptible categories (SPVD scores 4 and 5), eliminating almost all the resistant genotypes (scores 1 and 2). Likewise, when two promising diallel families (`Tanzania' × `Bikilamaliya' and `Tanzania' × `Wagabolige') were graft inoculated with SPCSV and SPFMV at CIP, severe SPVD was observed in most of the progenies. Individual inoculation of these two families with SPCSV or SPFMV, and Mendelian segregation analysis for resistant vs. susceptible categories led us to hypothesize that resistance to SPCSV and SPFMV was conditioned by two separate recessive genes inherited in a hexasomic or tetradisomic manner. Subsequent molecular marker studies yielded two genetic markers associated with resistance to SPCSV and SPFMV. The AFLP and RAPD markers linked to SPCSV and SPFMV resistance explained 70% and 72% of the variation in resistance, respectively. We propose naming these genes as spcsv1 and spfmv1. Our results also suggest that, in the presence of both of these viruses, additional genes mediate oligogenic or multigenic horizontal (quantitative) effects in the progenies studied for resistance to SPVD.