Combining ability for resistance to Sweetpotato Feathery Mottle Virus (SPFMV) was evaluated in seven sweetpotato [Ipomoea batatas (L.) Lam] clones. A diallel mating design was used, which resulted in 16 full-sib families. Families were evaluated for SPFMV resistance under greenhouse conditions in a randomized complete-block design. Resistance was tested by grafting Ipomoea nil `Scarlet O' Hara' infected with the russet crack strain of SPFMV (RC-SPFMV) onto individual plants of the families being evaluated. Symptomless plants were further indexed by cleft grafting virus-free Ipomoea setosa Ker plants onto the tested plants. Those plants in which the virus was not recovered by this test were considered resistant. Analysis of variance for SPFMV resistance revealed significant general combining abilities (GCA). Two clones, DLP-886 and TN90.300, exhibited significant positive GCA for SPFMV resistance. No significant specific combining abilities (SCA) were detected among the crosses. Breeding for resistance to SPFMV should focus on careful selection of resistant parents. In addition, results suggest that additive gene action is important in resistance to SPFMV.
Elisa Mihovilovich, Humberto A. Mendoza, and Luis F. Salazar
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.
M. Mcharo, D. LaBonte, R.O.M. Mwanga, and A. Kriegner
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.
K.S. Ling, C.A. Clark, C. Kokkinos, J. R. Bohac, S.S. Hurtt, R. L. Jarret, and A. G. Gillaspie
Sweet potato virus disease (SPVD) is the most devastating virus disease on sweetpotato [Ipomoea batatas (L.) Lam] world wide, especially in East Africa. However, weather it is present in the U.S. is unknown. SPVD is caused by co-infection of sweetpotato feathery mottle virus (SPFMV) and sweetpotato chlorotic stunt virus (SPCSV). Presence of two other potyviruses, sweetpotato virus G (SPVG) and Ipomoea vein mosaic virus (IVMV) has also been confirmed in the U.S. Sweet potato leaf curl virus (SPLCV), a whitefly (Bemisia tabaci) transmitted Begomovirus, also has the potential to spread to commercial sweetpotato fields and poses a great threat to the sweetpotato industry. The U.S. collection of sweetpotato germplasm contains about 700 genotypes or breeding lines introduced from over 20 different countries. Newly introduced sweetpotato germplasm from foreign sources are routinely screened for major viruses with serology and graft-transmission onto indicator plants (Ipomoea setosa). However, a large portion of this collection including heirloom cultivars or old breeding materials has not been systemically screened for these major sweetpotato viruses. In this study, a total of 69 so-called heirloom sweetpotato PI accessions were evaluated for their virus status. We used Real-time PCR to detect five sweetpotato viruses, including four RNA viruses (SPCSV, SPFMV, SPVG, and IVMV) and one DNA virus (SPLCV). A multiplex Real-time RT-PCR system was developed to detect three RNA viruses (SPFMV, SPVG, and IVMV). Preliminary data indicated that about 15% of these heirloom sweetpotato germplasm carried at least one of these viruses tested. Details on virus infection status will be presented.
Douglas Miano, Don LaBonte, and Christopher Clark
Sweetpotato is an important staple food crop in Sub-Saharan Africa, with production being concentrated in East Africa, particularly around Lake Victoria. Productivity of the crop is greatly constrained by viral diseases. Four main viruses have consistently been detected from various surveys done in the region viz., sweetpotato feathery mottle virus (SPFMV), sweetpotato chlorotic stunt virus (SPCSV), sweetpotato mild mottle virus (Sp.m.MV), and sweetpotato chlorotic fleck virus (SPCFV). The most severe symptoms have been caused by co-infection with SPCSV and SPFMV, resulting in the synergistic sweetpotato virus disease (SPVD). Some local sweetpotato genotypes have been reported to recover from, or have localized distribution of SPVD, suggesting that the disease is not fully systemic. This has led to the suggestion that uninfected cuttings may be obtained from previously infected plants. Experiments were set to determine the possibility of obtaining cuttings long enough for propagation that are free from virus infection. This would form a basis for recommending to the local small-holder farmers of a way to reduce losses due to the disease. Field-grown sweetpotato vines were cut into three pieces (15, 15–30, and >30 cm from the apex) and tested for SPCSV and SPFMV. Nine genotypes were selected from a group of 21 local clones and used for this study. The two viruses were equally present in all the three sections of infected vines, indicating that it is not easy to obtain a virus-free cutting for field propagation from an infected vine. Virus assays in the past has mainly been limited to the use of serological methods. Use of PCR resulted in detection of begomoviruses infecting sweetpotatoes for the first time in the region.
Scovia Adikini, Settumba B. Mukasa, Robert O.M. Mwanga, and Richard W. Gibson
single or combination of Sweetpotato feathery mottle virus (SPFMV) and Sweetpotato chlorotic stunt virus (SPCSV) in a screenhouse environment. Evidence of virus movement into storage roots and root sprouts after infection by SPFMV and SPCSV under
Benard Yada, Phinehas Tukamuhabwa, Arthur Villordon, Agnes Alajo, and Robert O.M. Mwanga
). Genetic erosion threatens this diversity as a result of sweetpotato virus disease (SPVD) caused by dual infection of Sweetpotato feathery mottle virus ( Potyvirus; Potyviridae ) and Sweetpotato chlorotic stunt virus ( Crinivirus; Closteroviridae
Benard Yada, Gina Brown-Guedira, Agnes Alajo, Gorrettie N. Ssemakula, Robert O.M. Mwanga, and G. Craig Yencho
sweetpotato genotypes using morphological and SSR markers Intl. J. Agr. Biol. 12 33 38 Karyeija, R.F. Gibson, R.W. Valkonen, J.P.T. 1998 The significance of sweetpotato feathery mottle virus in subsistence sweetpotato production in Africa Plant Dis. 82 4 15
Keith O. Fuglie
the viruses of most economic importance include sweetpotato chlorotic stunt virus (SPCSV) that together with the ubiquitous sweetpotato feathery mottle virus (SPFMV) cause the most devastating disease, especially in sub-Saharan Africa and Latin America
Jim C. Cervantes-Flores, G. Craig Yencho, Kenneth V. Pecota, Bryon Sosinski, and Robert O.M. Mwanga
chlorotic stunt virus and sweetpotato feathery mottle virus is mediated by two separate recessive genes in sweetpotato J. Amer. Soc. Hort. Sci. 127 798 806 Paulson, R.E. Webster, J.M. 1972 Ultrastructure of