Nature of Resistance and Response of Sweetpotato to Sweetpotato Virus Disease
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Date
2001-07-26
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Sweetpotato virus disease (SPVD) is a devastating disease due to the dual infection and synergistic interaction of sweetpotato feathery mottle potyvirus (SPFMV) and sweetpotato chlorotic stunt crinivirus (SPCSV). This study was conducted to: 1) determine the inheritance of resistance to SPVD in sweetpotato; 2) estimate the nature of genetic variance; and 3) evaluate methods for screening large populations for resistance to SPVD. The genetic basis of resistance to SPVD was investigated in three studies. The first genetic study consisted of a randomized block design at two sites in Uganda, during 1998-2000, using 45 full-sib diallel (half) families of 10 parental clones varying in SPVD resistance. The second study also conducted in Uganda, examined progeny from 15 promising sweetpotato diallel families (1352 genotypes), while the third examined two of the most promising families (294 genotypes) from the same diallel at the International Potato Center (CIP), Lima, Peru. Genetic component analysis of the 45 diallel families showed significant general combining ability (GCA) and specific combining ability (SCA) effects for resistance to SPVD. GCA to SCA variance components ratios were large (0.51-0.87) and resistant parents exhibited high GCA, indicating that additive gene effects were predominant in the inheritance of resistance to SPVD and recovery. Use of a suitable sweetpotato genotype for increase of SPVD inoculum and modified cleft graft inoculation led to rapid progress in screening large populations for SPVD resistance. The distribution of SPVD scores in the promising families was skewed toward highly susceptible categories, in Uganda and Peru. Inoculation of the two families at CIP with either SPCSV or SPFMV, and Mendelian segregation analysis for resistant versus susceptible categories for the two viruses suggest that resistance to SPCSV and SPFMV is conditioned by two, separate recessive genes. In the proposed model for inheritance, the two genes are unlinked and they are inherited in a hexasomic or tetradisomic manner. Based on amplified fragment length polymorphism (AFLP) and quantitative trait (QTL) loci analyses we identified two AFLP unlinked markers associated with loci conferring resistance to SPCSV and SPFMV in these progenies. We propose spcsv1 and spfmv1 to be the names of the genes.
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Degree
PhD
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Horticultural Science
