The Kishmish vatkana×VRH 3082-1-42 cross-resulted in 1,185
progeny plants. Following natural infection under greenhouse conditions,
286 of these plants were determined to be PM-susceptible
and 899 PM-resistant. The ratio of susceptible to symptomless individuals
in the hybrid family was 3:1. Run1+, Ren1+ and Run1+/Ren1+
genotypes of identical symptomless phenotypes were identified
with molecular markers, whose discrimination using traditional
methods would require a long time and complicated procedures.
For MAS analysis, we randomly selected 411 plants from the 899
PM-resistant and 30 from the PM-susceptible progeny. We used
these plants to test whether PM-resistance co-segregated with
Ren1 and/or Run1 specific markers. To find markers that can be
used for routine genotyping in MAS, we evaluated SSR markers
linked to Ren1 and Run1. For Ren1-linked markers, we assayed
VMC9h4.2, VMCNg4e10.1, and UDV020a, which were determined
by Hoffmann et al. (2008) to be located at a genetic distance of
approximately 0.9cM from the Ren1 locus. For all three of these
markers, amplicon size differences allowed unambiguous distinction
of Ren1 and its homologous allele. Allele sizes for VMC9h4.2,
VMCNg4e10.1, and UDV020a for the progeny under study are
shown in Fig. 1. The three Ren1-linked alleles were always inherited
together, confirming their tight linkage (Hoffmann et al.,
2008) (Table 1). All plants that carrying the Ren1-linked markers
were resistant to PM, and none of the 30 PM-susceptible
plants inherited any of the marker alleles indicating PM resistance.