Resistance to Sweetpotato Chlorotic Stunt Virus and Sweetpotato Feathery Mottle Virus Is Mediated by Two Separate Recessive Genes in Sweetpotato

in Journal of the American Society for Horticultural Science
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  • 1 Department of Horticultural Science, North Carolina State University, 201 Kilgore Hall, Box 7609, Raleigh, NC 27695-7609
  • 2 Austrian Research Centers, Biotechnology Unit, A-2444 Seibersdorf, Austria
  • 3 Department of Horticultural Science, North Carolina State University, 201 Kilgore Hall, Box 7609, Raleigh, NC 27695-7609
  • 4 International Potato Center (CIP), Apartado 1558, Lima 12, Peru
  • 5 Department of Plant Pathology, North Carolina State University, 1414 Gardner Hall, Box 7616, Raleigh, NC 27695-7616
  • 6 Department of Horticultural Science, North Carolina State University, Vernon G. James Research and Extension Center, 207 Research Station Road, Plymouth, NC 27962

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.

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