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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.

Resistance to root-knot nematodes [Meloidogyne incognita (Kofoid & White) Chitwood] in sweetpotato [Ipomoea batatas (L.) Lam.] was studied in a mapping population consisting of 240 progeny derived from a cross between ‘Beauregard’, the predominant cultivar in the United States, and ‘Tanzania’, an African landrace. Quantitative trait loci (QTL) analyses to locate markers associated with resistance to root-knot nematodes (RKN) were performed using genetic maps based on parental segregation in ‘Beauregard’ and ‘Tanzania’ consisting of 726 and 947 single-dose amplified fragment length polymorphism (AFLP) markers, respectively. RKN resistance in the progeny was highly skewed with most of the progeny exhibiting medium to high levels of resistance. Single-point analysis of variance and interval mapping revealed seven consistently significant QTL in ‘Tanzania’ and two significant QTL in ‘Beauregard’. In ‘Tanzania’, three QTL were associated with reduction in resistance as measured by the number of RKN egg masses and explained ≈20% of the variation. Another four QTL had positive effects on resistance and explained ≈21% of the variation. Other minor QTL explained ≈2% or less of the variation but were not always consistent across geographical locations. In ‘Beauregard’, two QTL had positive effects on RKN resistance and explained ≈6% of the observed variation. Based on molecular and phenotypic data, RKN resistance in sweetpotato is hypothesized to be conferred by several genes, but at least nine AFLP markers (seven from ‘Tanzania’ and two from ‘Beauregard’) are associated with genomic regions that have the biggest effect in the number of egg masses of RKN produced in the root system.