MOLECULAR MARKERS LINKED TO RHIZOMANIA RESISTANCE IN SUGAR-BEET, BETA-VULGARIS, FROM 2 DIFFERENT SOURCES MAP TO THE SAME LINKAGE GROUP

Rhizomania, one of the most important diseases of sugar beet, is cause d by beet necrotic yellow vein virus, a Furovirus vectored by the fung us Polymyxa betae Keskin. Reduction of the production losses caused by this disease can only be achieved by using tolerant cultivars. The ob jec tive of this study was the identification and mapping of random am plified polymorphic DNA (RAPD) markers linked to a rhizomania resistan ce gene. The RAPD markers were identified using bulked segregant analy sis in a segregating population of 62 individuals derived by intercros sing plants of the resistant commercial hybrid GOLF, and the resistanc e locus was positioned in a molecular marker linkage map made with a d ifferent population of 50 GOLF plants. The resistance locus, Rr1, was mapped to linkage group III of our map of Beta vulgaris L. ssp. vulgar is, which consisted of 76 RAPDs, 20 restriction fragment length polymo rphisms (RFLPs), three sequence characterized amplified regions (SCARs ) and one sequence tagged site (STS). In total, 101 molecular markers were mapped over 14 linkage groups which spanned 688.4 cM with an aver age interval length of 8.0 cM. In the combined map, Rr1 proved to be f lanked by the RAPD loci RA411(1800) and AS7(1100), at 9.5 and 18.5 cM, respectively. Moreover, in our I-2 population, we found that a set of markers shown by Barzen et al. (1997) to be linked to the 'Kolly' typ e resistance gene was also linked to the 'GOLF'-type resistance gene. These results appeared to indicate that the rhizomania resistance gene present in the GOLF hybrid could be the same gene underlying resistan ce in 'Rolly'-based resistant genotypes. Two other explanations could be applied: first, that two different alleles at the same locus could have been selected; second, that two different genes at two different but clustered loci underwent the selection process.