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Cecilia E. McGregor, Douglas W. Miano, Don R. LaBonte, Mary Hoy, Chris A. Clark and Guilherme J.M. Rosa

). Viruses are arguably responsible for the most damaging diseases in sweetpotato ( Clark et al., 1997 ; Fuglie, 2007 ; Gibson et al., 1997 ), and mixed infections are common ( Colinet et al., 1998 ). Sweet potato virus disease (SPVD) can lead to yield

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Robert O.M. Mwanga, Benson Odongo, Charles Niringiye, Agnes Alajo, Putri E. Abidin, Regina Kapinga, Silver Tumwegamire, Berga Lemaga, James Nsumba and Edward E. Carey

children and women. The cultivars have low to moderate levels of field resistance to sweetpotato virus disease (SPVD) and Alternaria blight ( Tables 2 and 3 ) and high storage root yields compared with the average national root yield of 4 t·ha −1

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R.O.M. Mwanga, B. Odongo, G. Turyamureeba, A. Alajo, G.C. Yencho, R.W. Gibson, N.E.J.M. Smit and E.E. Carey

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R.O.M. Mwanga, B. Odongo, C. Ocitti p'Obwoya, R.W. Gibson, N.E.J.M. Smit and E.E. Carey

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Fekadu Gurmu, Shimelis Hussein and Mark Laing

butterfly). SPVD is one of the major problems of sweetpotato production and productivity in east Africa where it is reported every cycle of production ( Karyeija et al., 1998 ). In addition, enhancing the nutritional traits of sweetpotato varieties is

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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.

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C.D. Kokkinos, C.A. Clark, C.E. McGregor and D.R. LaBonte

Sweet potato virus disease (SPVD) is the most devastating disease of sweetpotato [Ipomoea batatas (L.) Lam.] globally. It is caused by the co-infection of plants with a potyvirus, sweet potato feathery mottle virus (SPFMV), and a crinivirus, sweet potato chlorotic stunt virus (SPCSV). In this study we report the use of cDNA microarrays, containing 2765 features from sweetpotato leaf and storage root libraries, in an effort to assess the effect of this disease and its individual viral components on the gene expression profile of I. batatas cv. Beauregard. Expression analysis revealed that the number of differentially expressed genes (P < 0.05) in plants infected with SPFMV alone and SPCSV alone compared to virus-tested (VT) plants was only 3 and 14, respectively. However, these findings are in contrast with SPVD-affected plants where more than 200 genes were found to be differentially expressed. SPVD-responsive genes are involved in a variety of cellular processes including several that were identified as pathogenesis- or stress-induced.

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D.W. Miano, D. R. LaBonte and C. A. Clark

Sweet potato virus disease (SPVD) is a major constraint to sweetpotato production in East Africa. The disease is a result of co-infection with sweet potato feathery mottle virus (SPFMV) and sweet potato chlorotic stunt virus (SPCSV). 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 to 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.

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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.

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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.