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Sugar-beet powdery mildew, caused by the fungus Erysiphe betae, now occurs in all sugar-beet growing areas and can reduce sugar yield by up to 30%. Powdery mildew resistant plants from three novel sources were crossed with sugar beet to generate segregating populations. Evaluation of resistance was carried out in artificially inoculated field and controlled environment tests. The resistance level in two of the sources was found to be significantly higher than that in currently available sugar-beet cultivars. AFLP analysis was used in combination with bulked segregant analysis to develop markers linked to the resistant phenotype in each population. Five dominant major resistance genes were identified and assigned the proposed symbols Pm2 to Pm6. Pm3 conferred complete resistance to powdery mildew; the other genes conferred high levels of partial resistance. From the use of anchoring SNP markers, two genes were located to chromosome II and three to chromosome IV. Two of the genes on chromosome IV mapped to the same location and one of the genes on chromosome II mapped to the same region as the previously identified Pm1 gene. With the availability of these genes there is now excellent potential for achieving durable resistance to sugar-beet powdery mildew, thus reducing or obviating the need for chemical control.

An experiment was set up in 1998 to study the effect of glyphosate on the weeds and pests in glyphosate-tolerant sugar beet, in comparison with a conventional herbicide regime. Glyphosate at 1.08 kg ha À1 was ®rst applied at the two-to four-leaf, 8-to 10-leaf and 12-to 14-leaf stage of the crop, followed by a second application at the same rate two to four weeks later. Weed growth did not affect sugar beet emergence or establishment, but, in untreated controls and the two later glyphosate treatments, weeds almost completely covered the ground, leading to reduction of root weight, sugar concentration and yield at harvest. The number of aphids (mostly Myzus persicae Sulzer) in the beet in June was signi®cantly higher on plots treated with glyphosate at the two-to four-leaf stage than on untreated plots or plots treated later with glyphosate. Large numbers of the leaf curling plum aphid (Brachycaudus helichrysi Kaltenbach) colonised the weeds within untreated or later-treated plots. These were accompanied by predators and parasites which eventually caused substantial mortality in the aphid populations. There was evidence that glyphosate-treated weeds, although not in competition with the crop, were still able to provide sustenance for aphids. Very low levels of virus yellows were observed in the trial, and there were no signi®cant differences between treatments. The results suggest that the latest application of the ®rst glyphosate spray in a two-spray programme should be before the eight-leaf stage of the sugar beet to prevent weed competition reducing yield. Further studies on late control of weeds and insect diversity are being carried out.

Beet yellows virus (BYV) can dramatically reduce yield from sugar beet crops. A BYV resistant plant from a Beta germplasm accession was crossed with a sugar beet plant to generate the segregating population BYV1. This population was evaluated for BYV resistance and analysed with amplified fragment length polymorphism and singlenucleotide polymorphism markers to identify resistance loci. At 2 weeks after inoculation a number of plants displayed either mosaic or vein-clearing disease symptoms on infected leaves. The locus that largely controlled this disease reaction was mapped to chromosome IV. We refer to this novel genetic locus as Vc1. Three BYV resistance quantitative trait loci (QTLs) were identified and mapped to chromosomes III, V and VI. QTL mapping results suggested that the chromosome III and V QTLs acted only in plants with mosaic symptoms and that the chromosome VI QTL acted only in plants with the mosaic symptom allele of Vc1. These findings agreed with further statistical tests using general linear model analysis. There is now the potential to breed for BYV resistance using molecular marker technology.