Interval mapping of quantitative trait loci for corky ringspot disease resistance in a tetraploid population of potato (Solanum tuberosum subsp. tuberosum)

Corky Ringspot (CRS) disease is caused by Tobacco rattle virus and causes damage to both commercial and seed potato production. The genetics of resistance to CRS disease have not been clearly defined. The objectives of this study were to (1) determine the broad sense heritability of CRS resistance, (2) construct a linkage map for a tetraploid potato population expected to segregate for CRS resistance, and (3) determine the map position(s) of the quantitative trait loci (QTL) for CRS resistance. Three tetraploid potato populations consisting of 92 (population I), 91 (population II), and 89 (population III) genotypes were tested for CRS resistance in a CRS-infected field for four years (population II and III were tested for three years). Broad sense heritability and its standard error of CRS disease resistance for these populations was 0.72 (+/-0.149) for population I, 0.74 (+/-0.15) for population II, and 0.71 (+/-0.154) for population III. Population I crossing between PA95A33-1 (female, resistant) and A9446-7 (male, susceptible) was used to generate AFLP, SSR, and SSCP molecular marker profiles from which to construct molecular genetic maps for each parent. The total map length of PA95A33-1 was 2940 cM, with an average composite map length for each chromosome of 91.2 cM. The total map length of A9446-7 was 1929 cM, with an average composite map length for each chromosome of 79.6 cM. The PA95A33-1 map length of, 2940 cM represented approximately 73.5% coverage of genome. One major QTL that explained 43% of the phenotypic variation in CRS resistance was localized on chromosome IX, with flanking AFLP markers AAC-CGT-0347 and ACG-CTG-0588. A minor QTL that explained 12% of CRS resistance was also detected. This minor QTL was associated with distorted marker GGT-CAC-0259 which remained unlinked. The total additive effect of the major and minor QTLs explained more than 55% (43% from main QTL plus more than 12.3% from minor QTL) of the phenotypic variation. This number is a large portion of the 72% of total genetic variation in population 1. Conversion of the three mentioned AFLP markers to simple PCR markers will benefit resistance breeding by enabling marker assisted selection.