Epidemiology of beet necrotic yellow vein virus in sugar beet at different initial inoculum levels in the presence or absence of irrigation

A field experiment was set up in 1988 to study the development of rhizomania disease of sugar beet at different inoculum levels of beet necrotic yellow vein virus (BNYVV) in soil. Five, tenfold different, inoculum levels were created by addition of the approximate amounts of 0, 0.5, 5, 50 and 500 kg infested soil per ha (the latter corresponding to 0.01% v/v calculated to the tillage layer). A drip irrigation treatment was applied to study the influence of soil moisture on disease. Susceptible sugar beet, cv. Regina, was grown for three consecutive years.In the first year, root symptoms were not observed, but BNYVV-infected plants were detected by ELISA in low numbers at all inoculum levels at harvest. After late drilling in 1989, high numbers of infected plants, up to 90–100% in plots with the highest inoculum level, were detected already in June. Root symptoms were also observed from June onwards. In both these years disease incidence increased in time and was significantly influenced by the initial inoculum level. In the third year, the whole field was heavily diseased, and only for the non-irrigated plots incidence differed for different initial inoculum levels. The expression of symptoms by BNYVV-infected plants was influenced by initial inoculum level, thus by the amount and timing of primary infection.Root weight at harvest was not affected, but sugar content decreased with increasing inoculum level already in 1988, leading to a reduction in sugar yield of 10% at the highest inoculum level. In 1989, both root weight and sugar content decreased progressively with increasing inoculum level, resulting in sugar yield reductions of 11–66% (down to approximately 3000 kg ha^–1) for low to high inoculum levels compared to the control. As the control plots became contaminated, all yields were low in 1990, still showing a decrease with increasing inoculum level in the non-irrigated plots, but an overall mean sugar yield of 3323 kg ha^–1 for the irrigated ones.Sodium and -amino nitrogen content of the root, additional quality parameters determining extractability of sucrose, showed an increase and decrease, respectively, with increasing initial inoculum level already in the first year. The relative differences in contents compared to those from the control were largest for Na content. A significant negative correlation was found between Na (mmol kg^–1 root) and sugar content (% of fresh weight); linear for 1988, exponential for 1989 and 1990.In spring 1989, the infestation of individual plots was assessed using a quantitative bioassay estimating most probable numbers (MPNs) of infective units of BNYVV per 100 g dry soil. The relationship between the MPns determined and root weight, sugar content and sugar yield at harvest could be described by Gompertz curves. The increase in disease incidence with increasing MPN in 1989 was adequately fitted with a logistic equation.     

甜菜抗(耐)丛根病生理基础的研究(Ⅰ)过氧化物酶(POX)、多酚氧化酶(PPO)、苯丙氨酸解氨酶(PAL)与甜菜抗丛根病的关系

本文从比较生理学角度,研究了甜菜抗丛根病特性与其体内有关防御酶系的关系,结果表明,甜菜感病后,POX酶活性增加与抗病性有关,特别是PAL活性提高与抗病性呈正相关,可作为病地上和无病地上选育抗(耐)丛根病品种的重要生理指标.     

Epidemiology of beet necrotic yellow vein virus in sugar beet at different initial inoculum levels in the presence or absence of irrigation: Dynamics of inoculum

Using field plots where rhizomania had not previously been detected, different inoculum levels of beet necrotic yellow vein virus (BNYVV) were created by application of infested soil. A susceptible sugar beet cultivar (cv. Regina) was grown for two consecutive years (1988 and 1989), in the presence or absence of drip irrigation. In soil samples taken in spring 1989, the different initial inoculum levels of 1988 could be distinguished using a quantitative bioassay estimating most probable numbers (MPNs) of infective units per 100 g dry soil. The first sugar beet crop resulted in a tenthousandfold multiplication of inoculum of BNYVV (viruliferousPolymyxa betae). Mean MPNs of BNYVV ranged from 0.6 and 7 per 100 g soil for the lowest inoculum level to 630 and 1100 per 100 g for the highest level, in plots without and with irrigation, respectively. In spring 1990, MPNs had again increased. In both years, the initial inoculum level of 1988 had a significant linear effect on log-transformed MPNs of BNYVV determined. Log-transformed MPNs for 1990 and 1989 showed a positive linear correlation, despite a decreasing multiplication ratio at higher inoculum levels. Drip irrigation during one or two years enhanced the increase in MPN of BNYVV, which was reflected by the enhancement of multiplication ratios at all inoculum levels. The totalP. betae population was also higher after growing two irrigated crops than after growing two non-irrigated ones.     

Molecular markers linked to rhizomania resistance in sugar beet, Beta vulgaris, from two different sources map to the same linkage group

Rhizomania, one of the most important diseases of sugar beet, is caused by beet necrotic yellow vein virus, a Furovirus vectored by the fungus Polymyxa betae Keskin. Reduction of the production losses caused by this disease can only be achieved by using tolerant cultivars. The objective of this study was the identification and mapping of random amplified polymorphic DNA (RAPD) markers linked to a rhizomania resistance gene. The RAPD markers were identified using bulked segregant analysis in a segregating population of 62 individuals derived by intercrossing plants of the resistant commercial hybrid GOLF, and the resistance locus was positioned in a molecular marker linkage map made with a different population of 50 GOLF plants. The resistance locus, Rr1, was mapped to linkage group III of our map of Beta vulgaris L. ssp. vulgaris, which consisted of 76 RAPDs, 20 restriction fragment length polymorphisms (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 average interval length of 8.0 cM. In the combined map, Rr1 proved to be flanked by the RAPD loci RA411₁₈₀₀ and AS7₁₁₀₀ at 9.5 and 18.5cM, respectively. Moreover, in our I₂ population, we found that a set of markers shown by Barzen et al. (1997) to be linked to the ‘Holly’ type 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 resistance in ‘Holly’-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.     

Chromosome localisation of genes for resistance to Heterodera schachtii, Cercospora beticola and Polymyxa betae using sets of Beta procumbens and B. patellaris derived monosomic additions in B. vulgaris

Beet cyst nematodes (BCN, Heterodera schachtii), Cercospora beticola, and rhizomania, caused by the beet necrotic yellow vein virus (BNYVV) and vectored by the soil-borne fungus Polymyxa betae, are the most serious diseases of sugar beet ( Beta vulgaris subsp. vulgaris). The wild Beta species of section Procumbentes are known to be completely resistant to H. schachtii, C. beticola and P. betae. Alien monosomic additions (2n=19), plants of cultivated beet (2n=18) carrying different individual chromosomes of B. procumbens (2n=18) or B. patellaris (2n=36), were tested in greenhouse experiments for resistance to these pathogens. Gene(s) conferring full resistance to the beet cyst nematode in B. patellaris are located on chromosome 1.1, and the other tested chromosomes of B. patellaris are not involved in the expression of resistance. Artificial inoculation under greenhouse conditions, with in vitro produced inoculum of C. beticola and spot-percentage rating of the disease intensity, showed that the high level of resistance that was observed in the wild species B. procumbens and B. patellaris was not found in any of the monosomic additions tested. It was suggested that genes on various chromosomes of the wild species are needed to express full resistance, and that the chromosomes of group 7 of B. patellaris and chromosome 7 of B. procumbens have the largest effect. The greenhouse tests for resistance to P. betae in B. patellaris derived monosomic additions showed that the addition families of group 4.1 have a strong partial resistance, while the addition families of group 8.1 appeared to be completely resistant to the pathogen. Resistance to P. betae in the two wild species as well as in the two resistant addition types did not exclude infection with BNYVV, but resulted in a considerable reduction of the virus concentration. It was concluded that resistance to the vector would complement virus resistance, and may provide a more effective and durable control of rhizomania. This revised version was published online in July 2006 with corrections to the Cover Date.     

Reduced titer of BNYVV in transgenic sugar beets expressing the BNYVV coat protein

Summary Rhizomania is a disease of sugar beet caused by the furovirus beet necrotic yellow vein virus (BNYVV). Coat protein mediated resistance has been reported for a number of viral diseases. This approach to virus resistance was therefore attempted for control of rhizomania. Two constructs of the coat protein gene of BNYVV were introduced into sugar beet by Agrobacterium-mediated transformation. The mRNA level was estimated to be 0.01% of the poly A⁺ RNA. Expression of the coat protein gene was under the detection limit of our western blotting protocol i.e. below 0.01 g/50 g (0.02% of the total soluble protein). One transformation event per construct was tested in a greenhouse assay and in rhizomania infested soil in a field trial. In the greenhouse assay, transgenic plants showed a strong reduction of virus multiplication when compared to non-transgenic plants. This result was confirmed in the field trial, where a significant difference in virus multiplication was shown between plants with and without the coat protein gene.     

Modelling the effect of temperature on the development of Polymyxa betae

Polymyxa betae is the fungal vector of beet necrotic yellow vein virus (BNYVV), which is the causal agent of the sugar beet disease rhizomania. The within-season dynamics of the fungus are a crucial factor in the occurrence and severity of rhizomania. Late infection of the host by viruliferous fungi enables host resistance to the virus to develop and hence limits crop damage. A previously published mechanistic model for the dynamics of Polymyxa betae is extended in this paper to incorporate the effect of temperature on the germination of resting spores, and on the latent periods between infection and the production of secondary zoospores and new resting spores. It is shown that, for UK temperature conditions, the effect of sowing date on infection is greater than that of year-to-year variations in temperature associated with a single representative sowing date. The variation in inoculum build-up predicted when temperature data from a range of soil types were used in the model agreed with field observations, where higher levels of infection are observed on sandy soils than on black fen peat soils. The difference was most distinct when daily maximum soil temperature values were used to drive the model rather than rolling 24-hour average values.     

First Record of A and B Type Beet necrotic yellow vein virus in Sugar Beets in Sweden

Natural infections of sugar beet with Beet necrotic yellow vein virus (BNYVV), the causal agent of rhizomania, have been detected for the first time in Sweden in two small areas, one on the island of Öland and one in the Southeastern part of Scania. Single strand conformation polymorphism analyses of PCR products revealed that the infections on Öland were produced by A type BNYVV, whereas those in Scania were caused by the B type. This suggests that BNYVV has been introduced into Sweden at least twice. Alternatively, the virus may have invaded sugar beet from unknown native hosts. BNYVV RNA 5 was not detected in the samples investigated.     

Breeding for resistance to rhizomania in sugar beet: A review

Currently rhizomania is the most important disease in sugar beet worldwide, and attack can lead to serious yield losses. The disease is caused by beet necrotic yellow vein virus (BNYVV) that is transmitted by the soil-borne fungus Polymyxa betae. Breeding sugar beet cultivars with resistance to rhizomania is regarded as the most appropriate way to enable continued production of this crop in BNYVV-infested fields and also to slow the spread of the disease. Breeding for resistance started with selection by scoring disease symptoms in field experiments. The development of non-destructive greenhouse tests, with determination of the virus concentration in rootlets using ELISA, has greatly improved the efficiency of selection. In this paper the impact of scientific research on the progress in breeding cultivars with resistance to rhizomania is reviewed. This includes the distribution, composition, and pathogenicity of the virus, the sources of resistance to virus and vector, the genetics of virus resistance, progress with breeding methods, and the use of molecular markers and pathogen-derived resistance. The yields and quality characteristics of recently introduced resistant cultivars now equal those of the commercial susceptible cultivars. This revised version was published online in July 2006 with corrections to the Cover Date.     

Identification and mapping of random amplified polymorphic DNA markers linked to a rhizomania resistance gene in sugar beet (Beta vulgaris L.) by bulked segregant analysis

Bulked segregant analysis was employed to identify random amplified polymorphic DNA (RAPD) markers linked to a gene that confers rhizomania resistance to a sugar beet line created from a Holly Sugar Company breeding population (USA). Polymorphism revealed with 160 arbitrary 10-mer oligonucleotide primers was screened in two bulks produced by separately pooling the individual DNAs from the six most resistant and the six most susceptible plants of an F₂ population segregating for rhizomania resistance. A study of the F₂ individuals showed that 19 primers generated 44 polymorphic markers which were then grouped into nine linkage groups. By analysis of variance, 12 were shown to have a significant effect upon the level of resistance and were mapped on a segment 22.3 cM long. A quantitative trait locus (QTL) of resistance was identified and located in a 4.6cM interval between two markers. It accounted for 67.4% of the observed variation and almost all the genetic variation. These results suggest that the identified QTL corresponds to a unique major gene conditioning the Holly resistance studied, which we have named Rz-l.