R. O. M. Mwanga, Department of Horticultural Science, North Carolina State University, 201 Kilgore Hall, Box 7609, Raleigh, NC 27695-7609, USA, and National Agricultural Research Organization (NARO), National Crops Resources Research Institute (NaCRRI), Box 7084, Kampala, Uganda;
G. C. Yencho, Department of Horticulture, 214A Kilgore Hall, Box 7609, Raleigh, NC 27695-7609, USA;
R. W. Gibson, Natural Resources Institute, University of Greenwich, Central Avenue, Chatham Maritime, Kent, ME4 4TB, United Kingdom; and
J. W. Moyer, Department of Plant Pathology, North Carolina State University, 1414 Gardner Hall, Box 7616, Raleigh, NC 27695-7616, USA
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Accepted for publication 10 July 2012.
Evaluating sweetpotato (Ipomoea batatas) genotypes for resistance to sweetpotato virus disease (SPVD) has been slow and inefficient. Ipomoea setosa plants, normally used as the source of scions for graft-infecting sweetpotatoes with viral diseases, are often severely stunted and their mortality is 10 to 30% when infected with SPVD, making them unsuitable as scions. Tanzania, a landrace of I. batatas widely grown in East Africa, was found to be a superior host for maintaining and increasing SPVD inoculum (scions) for mass grafting. Modifications to a cleft-grafting technique also increased survival of grafted SPVD-affected scions from 5 to 100%. These modifications, coupled with an efficient SPVD scoring technique, allowed rapid screening of large sweetpotato populations for SPVD resistance. Plant recovery from SPVD is reported here as a component of SPVD resistance. Differences in recovery from SPVD were detected among progenies, indicating its genetic basis. Plant tip dieback, a hypersensitivity response, was observed only in families with cv. Wagabolige as a parent. These findings may open up new opportunities for improved understanding and control of this devastating disease.
© 2013 The American Phytopathological Society