Confirmation of the effectiveness and genetic positions of disease resistance loci in ‘Kishmish Vatkana’ (Ren1) and ‘Villard Blanc’ (Ren3 and Rpv3)

Abstract

This study aimed to validate the effectiveness and to genetically characterise the fungal disease resistance genes of 'Kishmish Vatkana' and 'Villard Blanc' in South Africa using microsatellite (SSR) markers and a Quantitative Trait Loci (QTL) approach. An F 1 'Sunred Seedless' × 'Kishmish Vatkana' cross was used to generate a partial linkage map for chromosome 13 known to harbour the Ren1 powdery mildew locus of 'Kishmish Vatkana'. The effectiveness of this locus was validated, explaining between 44.8% and 57.7% of the observed phenotypic variance. An F 1 'Villard Blanc' × 'G1-6604' cross was used to generate partial linkage maps for chromosomes 15 and 18, reported to harbour fungal resistance genes of 'Villard Blanc'. The powdery mildew QTL (Ren3) was validated on chromosome 15 of 'Villard Blanc', which explained between 18.9% and 23.9% of the phenotypic variance observed. The downy mildew resistance QTL on chromosome 18 (Rpv3) of 'Villard Blanc' was also confirmed, and it explained between 19.1% and 21.2% of the phenotypic variance observed. This molecular information and individual sources of resistance have already been implemented in the marker-assisted selection (MAS) and gene pyramiding efforts of the table grape breeding program of the Agricultural Research Council (ARC) Infruitec-Nietvoorbij.

Confirmation and Fine Mapping of the Resistance Locus Ren9 from the Grapevine Cultivar ‘Regent’

“…The QTL results for this date show a QTL-region flanked by the markers UDV-116/GF15-30 and GF15-42/ScOR-A7 ( Figure 2 ). This region agrees with the previously published localization of locus Ren3 [ 16 , 23 ] and confirms it in this independent mapping study. The phenotypic scores of genotypes without any R -locus are shifted towards susceptible from the second scoring date onwards ( Figure 1 , 16-2 to 16-4) reflecting the developing PM epidemic and increasing infection pressure.…”

“…In another study, the same research team showed the Ren3 QTL associated with marker UDV-116, which is located in the middle of chromosome 15. One could argue that if the marker density in the anterior part of chromosome 15 would have been increased, the QTL would have been possibly shifted further to the beginning of the chromosome [ 23 ]. Teh et al [ 24 ] also investigated the resistance Ren3 with a SNP based genetic map and phenotypic field data.…”