SUMMARY Leaf spot disease caused by Cercospora beticola Sacc. is the most destructive foliar pathogen of sugarbeet worldwide. In addition to reducing yield and quality of sugarbeet, the control of leaf spot disease by extensive fungicide application incurs added costs to producers and repeatedly has selected for fungicide‐tolerant C. beticola strains. The genetics and biochemistry of virulence have been examined less for C. beticola as compared with the related fungi C. nicotianae, C. kikuchii and C. zeae‐maydis, fungi to which the physiology of C. beticola is often compared. C. beticola populations generally are not characterized as having race structure, although a case of race‐specific resistance in sugarbeet to C. beticola has been reported. Resistance currently implemented in the field is quantitatively inherited and exhibits low to medium heritability. Taxonomy: Cercospora beticola Sacc.; Kingdom Fungi, Subdivision Deuteromycetes, Class Hyphomycetes, Order Hyphales, Genus Cercospora. Identification: Circular, brown to red delimited spots with ashen‐grey centre, 0.5–6 mm diameter; dark brown to black stromata against grey background; pale brown unbranched sparingly septate conidiophores, hyaline acicular conidia, multiseptate, from 2.5 to 4 µm wide and 50–200 µm long. Host range: Propagative on Beta vulgaris and most species of Beta. Reported on members of the Chenopodiaceae and on Amaranthus. Disease symptoms: Infected leaves and petioles of B. vulgaris exhibit numerous circular leaf spots that coalesce in severe cases causing complete leaf collapse. Dark specks within a grey spot centre are characteristic for the disease. Older leaves exhibit a greater number of lesions with larger spot diameter. During the latter stage of severe epiphytotics, new leaf growth can be seen emerging from the plant surrounded by prostrate, collapsed leaves. Control: Fungicides in the benzimidazole and triazole class as well as organotin derivatives and strobilurins have successfully been used to control Cercospora leaf spot. Elevated levels of tolerance in populations of C. beticola to some of the chemicals registered for control has been documented. Partial genetic resistance also is used to reduce leaf spot disease.

A panel of 13 sugar beet lines and one genotype each of the Beta vulgaris cultivars red beet and Swiss chard, and B. vulgaris ssp. maritima were used to identify polymorphisms in alignments of genomic DNA sequences derived from 315 EST- and 43 non-coding RFLP-derived loci. In sugar beet lines, loci of expressed genes showed an average SNP frequency of 1/72 bp, 1 in 58 bp in non-coding sequences, increasing to 1/47 bp upon the addition of the remaining genotypes. Within analysed DNA fragments, alleles at different SNP positions displayed linkage disequilibrium indicative of haplotype structures. On average 2.7 haplotypes were found in sugar beet lines, and haplotype conservation in expressed genes appeared to exceed 500 bp in length. Seven different genotyping techniques including SNP detection by MALDI-TOF mass spectrometry, pyrosequencing and fluorescence scanning of labelled nucleotides were employed to perform 712 segregation analyses for 538 markers in three F(2) populations. Functions were predicted for 492 mapped sequences. Genetic maps comprised 305 loci covering 599.8 cM in population K1, 241 loci distributed over 636.6 cM in population D2, and 166 loci over 507.1 cM in population K2, respectively. Based on 156 markers common to more than one population an integrated map was constructed with 524 loci covering 664.3 cM. For 377 loci the genome positions of the most similar sequences from A. thaliana were identified, but little evidence for previously presented ancestral genome structures was found.

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Rhizoctonia root and crown rot caused by the fungus Rhizoctonia solani is a serious disease of sugar beet. An F 2:3 population from a cross between a resistant and a susceptible parent has been tested for R. solani resistance and a genetic map has been constructed from the corresponding F 2 parents. The map encompasses 38 expressed sequence tags (ESTs) with high similarity to genes which are involved in resistance reactions of plants (R-ESTs) and 25 bacterial artificial chromosomes (BACs) containing nucleotide binding site (NBS)-motifs typical for disease resistance genes. Three quantitative trait loci (QTL) for R. solani resistance were found on chromosomes 4, 5 and 7 collectively explaining 71% of the total phenotypic variation. A number of R-ESTs were mapped in close distance to the R. solani resistance QTL. In contrast, the NBS-BACs mapped to chromosomes 1, 3, 7 and 9 with two major clusters of NBS-BACs on chromosome 3. No linkage between NBS-BACs and R. solani resistance QTL was found. The data are discussed with regard to using R-ESTs and NBS markers for mapping quantitative disease resistances.

Worldwide, rhizomania is the most important disease of sugar beet. The only way to control this disease is to use resistant varieties. Four full-length resistance gene analogues (RGAs) from sugar beet (cZR-1, cZR-3, cZR-7, and cZR-9) were used in this study. Their predicted polypeptides carry typical nucleotide-binding sites (NBSs) and leucin-rich repeat (LRR) regions, and share high homology to various plant virus resistance genes. Their corresponding alleles were cloned and sequenced from a rhizomania resistant genotype. The 4 RGAs were mapped as molecular markers, using sequence-specific primers to determine their linkage to the rhizomania resistance locus Rz1 in a population segregating for rhizomania resistance. One cZR-3 allele, named Rz-C, together with 5 other molecular markers, mapped to the Rz1 locus on chromosome 3 and cosegregated with quantitative trait loci for rhizomania resistance. After screening a bacterial artificial chromosome (BAC) library, 25 cZR-3-positive BACs were identified. Of these, 15 mapped within an interval of approximately 14 cM on chromosome 3, in clusters close to the Rz1 locus. Rz-C differentiates between susceptible and resistant beet varieties, and its transcripts could be detected in all rhizomania resistant varieties investigated. The potential of this RGA marker for cloning of rhizomania resistance genes is discussed.