Five sweetpotato [Ipomoea batatas (L.) Lam.] cultivars (`Beauregard', `Excel', `Jewel', `Hernandez', and `Porto Rico') were evaluated for resistance to three root-knot nematode species: Meloidogyne arenaria (Neal) Chitwood (race 2), M. incognita (Kofoid & White) Chitwood (race 3), and M. javanica (Treub) Chitwood. Resistance screening efficiency was assessed in both 400-cm3 square pots and 150-cm3 Conetainers™. Nematode infection was assessed as the percentage of root system galled, percentage of root system necrosis, and the number of nematode eggs produced per gram of root tissue. Means of these dependent variables were not different (P ≤ 0.05) between container types, with Conetainers™ being more efficient to use. Root necrosis was not related to nematode infection, but was significant among cultivars (P = 0.0005). The resistance responses of the cultivars differed depending on the nematode species. All five cultivars were resistant to M. arenaria race 2. `Hernandez', `Excel', and `Jewel' were also resistant to M. incognita race 3 and M. javanica.
J.C. Cervantes-Flores, G.C. Yencho and E.L. Davis
J.C. Cervantes-Flores, G.C. Yencho and E.L. Davis
Sweetpotato [Ipomoea batatas (L.) Lam.] genotypes were evaluated for resistance to North Carolina root-knot nematode populations: Meloidogyne arenaria (Neal) Chitwood races 1 and 2; M. incognita (Kofoid & White) Chitwood races 1, 2, 3, and 4; and M. javanica (Treub) Chitwood. Resistance screening was conducted using 150-cm3 Conetainers containing 3 sand: 1 soil mix. Nematode infection and reproduction were assessed as the number of egg masses produced by root-knot nematodes per root system. Host suitability for the root-knot nematode populations differed among the 27 sweetpotato genotypes studied. Five genotypes (`Beauregard', L86-33, PDM P6, `Porto Rico', and `Pelican Processor') were selected for further study based on their differential reaction to the different root-knot nematodes tested. Two African landraces (`Tanzania' and `Wagabolige') were also selected because they were resistant to all the nematode species tested. The host status was tested against the four original M. incognita races, and an additional eight populations belonging to four host races, but collected from different geographical regions. The virulence of root-knot nematode populations of the same host race varied among and within sweetpotato genotypes. `Beauregard', L86-33, and PDM P6 were hosts for all 12 M. incognita populations, but differences in the aggressiveness of the isolates were observed. `Porto Rico' and `Pelican Processor' had different reactions to the M. incognita populations, regardless of the host race. Several clones showed resistance to all M. incognita populations tested. These responses suggest that different genes could be involved in the resistance of sweetpotato to root-knot nematodes. The results also suggest that testing Meloidogyne populations against several different sweetpotato hosts may be useful in determining the pathotypes affecting sweetpotato.
R.O.M. Mwanga, A. Kriegner, J.C. Cervantes-Flores, D.P. Zhang, J.W. Moyer and G.C. Yencho
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.