Item Details

Title: Nature of Resistance and Response of Sweetpotato to Sweetpotato Virus Disease

Date Published: 2001
Author/s: Robert O. Mwanga
Data publication:
Funding Agency :
Copyright/patents/trade marks:
Journal Publisher:
Affiliation: NARO
Keywords: Sweetpotato; Sweetpotato virus disease; SPVD; sweetpotato feathery mottle potyvirus; SPFMV

Abstract:

Sweetpotato virus disease (SPVD) is a devastating disease due to the dual infection and
synergistic interaction of sweetpotato feathery
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
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 (1852 genotypes), while the third examined two of the most promising
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
parents exhibited high GCA, indicating that additive gene effects
inheritance of resistance to SPVD and recovery. Use of a suitable sweetpotato genotype for
screening large populations for SPVD resistance. The distribution of SPVD scores in the
skewed toward highly susceptible categories, in Uganda and Peru.
mottle potyvirus (SPFMV) and sweetpotato
were predominant in the
promising families was
families (294 genotypes) from the same diallel at the International Potato Center (CIP),
increase of SPVD inoculum and modified cleft graft inoculation led to rapid progress in
SPVD. GCA to SCA variance components ratios were large (0.51-0.87) and resistant
chlorotic stunt crinivirus (SPCSV). This study was conducted to: 1) determine the Inoculation of the two families at CIP with either SPCSV or SPFMV, and Mendelian
that resistance to SPCSV and SPFMV is conditioned by two, separate recessive genes. In
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 spcsvl and spfmvl to be the names of the genes.