Quantitative trait loci associated with resistance to sweet potato virus disease in ‘Beauregard x Tanzania’ mapping population

Abstract

Sweetpotato (Ipomoea batatas (L.) Lam.) (2n = 6x = 90) is a major food security crop in sub Saharan Africa, consumed as a source of carbohydrate, proteins, minerals, vitamins E and B, and beta-carotene. Sweetpotato production is still greatly constrained by sweet potato virus disease (SPVD) with no reported genotype showing complete resistance. SPVD is caused by synergistic infection of Sweet potato feathery mottle virus (SPFMV) and Sweet potato chlorotic stunt virus (SPCSV). There is need to identify sources of resistance to SPVD, which can be achieved by understanding the genetic nature of resistance to be able to design the right breeding strategy. The objective of this study was to identify the segregation patterns and single nucleotide polymorphism (SNP) markers linked to loci controlling resistance to SPVD, SPCSV and SPFMV in a mapping population developed from a cross between cv. ‘Beauregard’ (B) (US bred) and cv. ‘Tanzania’ (T) (African landrace). Genotypes were evaluated using an augmented randomized complete block design laid out in a screenhouse with graft inoculation using infected Ipomoea setosa scions and the virus scores taken at different time intervals. The severity scores were used for quantitative trait loci (QTL) mapping using an integrated BT linkage map of length 2,708.4 cM comprising 30,684 SNP markers at a density of 11.35 markers per cM. A total of 13 genotypes showed superior performance compared to cv. ‘Tanzania’ for both SPVD and SPFMV with resistance genes following both hexasomic and tetradisomic patterns of inheritance. Using the random effect multiple interval mapping approach in the specialized software QTLpoly for polyploids, one major QTL explaining 14.82% of phenotypic variation of genotype reaction to SPVD was mapped on the linkage group 10. Three QTL all co-localized on linkage group 3 each explaining 16.73%, 17.11% and 19.82% of observed genotypes reaction to SPFMV were also identified in the BT mapping population. Both parents contributed favorable haplotypes with negative additive effects. Stress and pathogen response genes were identified within the QTL support intervals.