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Vicinal oxygen chelate (VOC) proteins are members of an enzyme superfamily with dioxygenase or non‐dioxygenase activities. However, the biological functions of VOC proteins in plants are poorly understood. Here, we show that a VOC in Nicotiana benthamiana (NbVOC1) facilitates viral infection. NbVOC1 was significantly induced by infection by beet necrotic yellow vein virus (BNYVV). Transient overexpression of NbVOC1 or its homolog from Beta vulgaris (BvVOC1) enhanced BNYVV infection in N. benthamiana, which required the nuclear localization of VOC1. Consistent with this result, overexpressing NbVOC1 facilitated BNYVV infection, whereas, knockdown and knockout of NbVOC1 inhibited BNYVV infection in transgenic N. benthamiana plants. NbVOC1 interacts with the basic leucine zipper transcription factors bZIP17/28, which enhances their self‐interaction and DNA binding to the promoters of unfolded protein response (UPR)‐related genes. We propose that bZIP17/28 directly binds to the NbVOC1 promoter and induces its transcription, forming a positive feedback loop to induce the UPR and facilitating BNYVV infection. Collectively, our results demonstrate that NbVOC1 positively regulates the UPR that enhances viral infection in plants. [ABSTRACT FROM AUTHOR]

This document provides the conclusions of the pest survey card that was prepared in the context of the EFSA mandate on plant pest surveillance (M‐2020‐0114) at the request of the European Commission. The full pest survey card for beet necrotic yellow vein virus is published and available online in the EFSA Pest Survey Card gallery at the following link and will be updated whenever new information becomes available: https://efsa.europa.eu/plants/planthealth/monitoring/surveillance/beet-necrotic-yellow-vein-virus [ABSTRACT FROM AUTHOR]

Sugar beet cultivation is dependent on an effective control of beet necrotic yellow vein virus (BNYVV, family Benyviridae), which causes tremendous economic losses in sugar production. As the virus is transmitted by a soilborne protist, the use of resistant cultivars is currently the only way to control the disease. The Rz2 gene product belongs to a family of proteins conferring resistance towards diverse pathogens in plants. These proteins contain coiled‐coil and leucine‐rich repeat domains. After artificial inoculation of homozygous Rz2 resistant sugar beet lines, BNYVV and beet soilborne mosaic virus (BSBMV, family Benyviridae) were not detected. Analysis of the expression of Rz2 in naturally infected plants indicated constitutive expression in the root system. In a transient assay, coexpression of Rz2 and the individual BNYVV‐encoded proteins revealed that only the combination of Rz2 and triple gene block protein 1 (TGB1) resulted in a hypersensitive reaction (HR)‐like response. Furthermore, HR was also triggered by the TGB1 homologues from BSBMV as well as from the more distantly related beet soilborne virus (family Virgaviridae). This is the first report of an R gene providing resistance across different plant virus families. [ABSTRACT FROM AUTHOR]

Summary: Many plant viruses with monopartite or bipartite genomes have been developed as efficient expression vectors of foreign recombinant proteins. Nonetheless, due to lack of multiple insertion sites in these plant viruses, it is still a big challenge to simultaneously express multiple foreign proteins in single cells. The genome of Beet necrotic yellow vein virus (BNYVV) offers an attractive system for expression of multiple foreign proteins owning to a multipartite genome composed of five positive‐stranded RNAs. Here, we have established a BNYVV full‐length infectious cDNA clone under the control of the Cauliflower mosaic virus 35S promoter. We further developed a set of BNYVV‐based vectors that permit efficient expression of four recombinant proteins, including some large proteins with lengths up to 880 amino acids in the model plant Nicotiana benthamiana and native host sugar beet plants. These vectors can be used to investigate the subcellular co‐localization of multiple proteins in leaf, root and stem tissues of systemically infected plants. Moreover, the BNYVV‐based vectors were used to deliver NbPDS guide RNAs for genome editing in transgenic plants expressing Cas9, which induced a photobleached phenotype in systemically infected leaves. Collectively, the BNYVV‐based vectors will facilitate genomic research and expression of multiple proteins, in sugar beet and related crop plants. [ABSTRACT FROM AUTHOR]

Summary: Rhizomania of sugar beet, caused by Beet necrotic yellow vein virus (BNYVV), is characterized by excessive lateral root (LR) formation leading to dramatic reduction of taproot weight and massive yield losses. LR formation represents a developmental process tightly controlled by auxin signaling through AUX/IAA‐ARF responsive module and LATERAL ORGAN BOUNDARIES DOMAIN (LBD) transcriptional network. Several LBD transcription factors play central roles in auxin‐regulated LR development and act upstream of EXPANSINS (EXPs), cell wall (CW)‐loosening proteins involved in plant development via disruption of the extracellular matrix for CW relaxation and expansion. Here, we present evidence that BNYVV hijacks these auxin‐regulated pathways resulting in formation LR and root hairs (RH). We identified an AUX/IAA protein (BvAUX28) as interacting with P25, a viral virulence factor. Mutational analysis indicated that P25 interacts with domains I and II of BvAUX28. Subcellular localization of co‐expressed P25 and BvAUX28 showed that P25 inhibits BvAUX28 nuclear localization. Moreover, root‐specific LBDs and EXPs were greatly upregulated during rhizomania development. Based on these data, we present a model in which BNYVV P25 protein mimics action of auxin by removing BvAUX28 transcriptional repressor, leading to activation of LBDs and EXPs. Thus, the evidence highlights two pathways operating in parallel and leading to uncontrolled formation of LRs and RHs, the main manifestation of the rhizomania syndrome. [ABSTRACT FROM AUTHOR]

Rhizomania is one of the most damaging and widely spread diseases in major sugar beet growing regions of the world. The causal agent, beet necrotic yellow vein virus ( BNYVV), is transmitted via the fungus Polymyxa betae, which retains it in the field for years. In this study, an RNA silencing mechanism was employed to induce resistance against rhizomania using intron-hairpin RNA (ihp RNA) constructs. These constructs were based on sequences of the BNYVV 5′-untranslated region of RNA-2 or the flanking sequence encoding P21 coat protein, with different lengths and orientations. Both transient and stable transformation methods produced effective resistance against rhizomania correlated with the transgene presence. Among the constructs, those generating ihp RNA structures with small intronic loops produced the highest frequencies of resistant events. The inheritance of transgenes and resistance was confirmed over generations in stably transformed plants. [ABSTRACT FROM AUTHOR]

Rhizomania, one of the most devastating diseases in sugar beet production, is caused by Beet necrotic yellow vein virus ( BNYVV) and transmitted by Polymyxa betae. Previously, disease control was possible by cultivation of sugar beet hybrids carrying a major resistance gene Rz1, which restricts virus accumulation in taproots and suppresses symptom development. Over the last few years, BNYVV strains with four RNA components have arisen, which are able to overcome Rz1-mediated resistance. All strains described so far possess an A67V amino acid exchange within the RNA3-encoded P25 pathogenicity factor. In this study, BNYVV was isolated from Rz1 plants, collected in the United Kingdom, the Netherlands and Germany, displaying patches of strong rhizomania symptoms. Sequencing of the coat protein and P25 gene of three isolates showed 100% nucleotide sequence identity and detected AYPR as the P25 tetrad amino acid composition. The ability of this strain to accumulate to higher levels in young plants of Rz1 resistant but not in Rz1 + Rz2 resistant genotypes was initially demonstrated in a greenhouse assay in natural field soil from the Netherlands. This strain was loaded into a virus-free P. betae population and compared to reference strains. The AYPR strain retained its resistance-breaking ability in the Rz1 genotypes and displayed replication at a higher rate compared to the Rz1-resistance-breaking P type. The strain origin is unclear and it remains speculative whether the occurrence at different geographic locations is the result of independent selection or displacement of infested soil. [ABSTRACT FROM AUTHOR]

Polymyxa betae is a biotrophic obligate sugar beet parasite that belongs to plasmodiophorids. The infection of sugar beet roots by this parasite is asymptomatic, except when it transmits Beet necrotic yellow vein virus ( BNYVV), the causal agent of rhizomania. To date, there has been little work on P. betae-sugar beet molecular interactions, mainly because of the obligate nature of the parasite and also because research on rhizomania has tended to focus on the virus. In this study, we investigated these interactions through differential transcript analysis, using suppressive subtractive hybridization. The analysis included 76 P. betae and 120 sugar beet expressed sequence tags ( ESTs). The expression of selected ESTs from both organisms was monitored during the protist life cycle, revealing a potential role of two P. betae proteins, profilin and a Von Willebrand factor domain-containing protein, in the early phase of infection. This study also revealed an over-expression of some sugar beet genes involved in defence, such as those encoding PR proteins, stress resistance proteins or lectins, especially during the plasmodial stage of the P. betae life cycle. In addition to providing new information on the molecular aspects of P. betae-sugar beet interactions, this study also enabled previously unknown ESTs of P. betae to be sequenced, thus enhancing our knowledge of the genome of this protist. [ABSTRACT FROM AUTHOR]

The control of rhizomania, one of the most important diseases of sugar beet caused by the Beet necrotic yellow vein virus, remains limited to varietal resistance. In this study, we investigated the putative action of Bacillus amylolequifaciens lipopeptides in achieving rhizomania biocontrol through the control of the virus vector Polymyxa betae. Some lipopeptides that are produced by bacteria, especially by plant growth-promoting rhizobacteria, have been found to induce systemic resistance in plants. We tested the impact of the elicitation of systemic resistance in sugar beet through lipopeptides on infection by P. betae. Lipopeptides were shown to effectively induce systemic resistance in both the roots and leaves of sugar beet, resulting in a significant reduction in P. betae infection. This article provides the first evidence that induced systemic resistance can reduce infection of sugar beet by P. betae. [ABSTRACT FROM AUTHOR]

Beet necrotic yellow vein virus ( BNYVV), vectored by Polymyxa betae, causes rhizomania in sugar beet. For disease control, the cultivation of hybrids carrying Rz1 resistance is crucial, but is compromised by resistance-breaking ( RB) strains with specific mutations in the P25 protein at amino acids 67-70 (tetrad). To obtain evidence for P25 variability from soil-borne populations, where the virus persists for decades, populations with wild-type ( WT) and RB properties were analysed by P25 deep sequencing. The level of P25 variation in the populations analysed did not correlate with RB properties. Remarkably, one WT population contained P25 with RB mutations at a frequency of 11%. To demonstrate selection by Rz1 and the influence of RB mutations on relative fitness, competition experiments between strains were performed. Following a mixture of strains with four RNAs, a shift in tetrad variants was observed, suggesting that strains did not mix or transreplicate. The plant genotype exerted a clear influence on the frequency of RB tetrads. In Rz1 plants, the RB variants outcompeted the WT variants, and mostly vice versa in susceptible plants, demonstrating a relative fitness penalty of RB mutations. The strong genotype effect supports the hypothesized Rz1 RB strain selection with four RNAs, suggesting that a certain tetrad needs to become dominant in a population to influence its properties. Tetrad selection was not observed when an RB strain, with an additional P26 protein encoded by a fifth RNA, competed with a WT strain, supporting its role as a second BNYVV pathogenicity factor and suggesting the reassortment of both types. [ABSTRACT FROM AUTHOR]

The plasmodiophoromycete Polymyxa betae is an obligate root parasite that transmits Beet necrotic yellow vein virus (BNYVV), the cause of sugar beet rhizomania disease. Currently, control of this disease is achieved through the use of cultivars with monogenic ( Rz1) partial resistance to the virus. To improve the level and durability of this resistance, sources of resistance to the virus vector, P. betae, were sought. Over 100 accessions of the wild sea beet ( Beta vulgaris ssp. maritima) from European coastal regions were evaluated for resistance in controlled environment tests. Quantification of P. betae biomass in seedling roots was achieved using recombinant antibodies raised to a glutathione-s-transferase expressed by the parasite in vivo. Several putative sources of resistance were identified and selected plants from these were hybridized with a male-sterile sugar beet breeding line possessing partial virus resistance ( Rz1). Evaluation of F1 hybrid populations identified five in which P. betae resistance had been successfully transferred from accessions originating from Mediterranean, Adriatic and Baltic coasts. A resistant individual from one of these populations was backcrossed to the sugar beet parent to produce a BC1 population segregating for P. betae resistance. This population was also tested for resistance to BNYVV. Amplified fragment length polymorphism and single-nucleotide polymorphism markers were used to map resistance quantitative trait loci (QTL) to linkage groups representing specific chromosomes. QTL for resistance to both P. betae and BNYVV were co-localized on chromosome IV in the BC1 population, indicating resistance to rhizomania conditioned by vector resistance. This resistance QTL ( Pb1) was shown in the F1 population to reduce P. betae levels through interaction with a second QTL ( Pb2) found on chromosome IX, a relationship confirmed by general linear model analysis. In the BC1 population, vector-derived resistance from wild sea beet combined additively with the Rz1 virus resistance gene from sugar beet to reduce BNYVV levels. With partial virus resistance already deployed in a number of high-yielding sugar beet cultivars, the simple Pb1/ Pb2 two-gene system represents a valuable additional target for plant breeders. [ABSTRACT FROM AUTHOR]

Abstract Production of sugar beet, the most important source of sugar in Syria, has suffered from many problems in the past, especially from diseases. No previous surveys have been made in Syria for viral diseases and soil-borne fungi of sugar beet. In 1998, samples were collected from plants showing symptoms of virus infection (yellowing, wilting, necrosis and mosaic). Root samples (341) were collected from crops of autumn-sown seed from 115 localities in seven provinces, 173 root samples from spring-sown crops and 39 leaf samples were collected during both seasons. The root samples were tested for the presence of viruses by double antibody sandwich-enzyme-linked immunosorbent assay (ELISA) and triple antibody sandwich-ELISA, and for soil-borne fungi by red plate (Rose Bengal) dishes. We have shown for the first time the presence of Beet necrotic yellow vein virus , Beet soil-borne virus , Beet yellows virus and Beet mild yellowing virus in Syrian sugar beet fields in which Rhizoctonia sp. and Fusarium sp. were also widely distributed. [ABSTRACT FROM AUTHOR]

The article presents a study on the effects of hybrids between transgenic sugar beets and Swiss chard using hand-crossing. Ecological implications are found to be observed only in feral Swiss chard and wild beet populations due to the spread of virus-resistant transgenic hybrids. Chenopodium album is also noted to negatively influence the performance of genotypes.

After infection with spores of a virulent strain of Ascochyta rabiei the chickpea (Cicer arietinum) cultivars ILC 1929 (susceptible) and ILC 3279 (resistant) were compared with regard to pterocarpan phytoalexin and isoflavone accumulation. Quantitative HPLC analyses of total extracts of aerial parts were used to measure the induced formation of the phytoalexins medicarpin and maackiain and the accumulation of the constitutive isoflavones biochanin A and formononetin together with their 7-0- glucosides and their 7-Q-glucoside-6"-0-malonates. The two cultivars showed no significant difference in the level of isoflavones and isoflavone conjugates. On the other hand, the resistant cultivar ILC 3279 rapidly accumulated large amounts of both phytoalexins (20--6 nmole g~* fr.w.) whereas cultivar ILC 1929 only produced very small amounts (5 nmole g"1 fr.w.) of medicarpin. The data are discussed with regard to isoflavonoid metabolism and the significance of induced and constitutive levels of phytoalexins and isoflavones in resistance of chickpea towards A. rabiei. [ABSTRACT FROM AUTHOR]

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 F[SUB2] population segregating for rhizomania resistance. A study of the F[SUB2] 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 4.6 cM 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-1. [ABSTRACT FROM AUTHOR]

Resistance to Polymyxa betae was studied in Beta species of the section Procumbentes, in hybrids of B. vulgaris with B. procumbens or B. patellaris, and in monosomic additions of chromosomes of B. procumbens in B. vulgaris. In all experiments P. betae infested with beet necrotic yellow vein virus (BNYVV) was used. This virus causes rhizomania in sugar beet, and the effect of vector resistance was studied by measuring virus concentrations. Cystosori of P. betae were not found in the wild species and the hybrids. Virus concentrations in these plants were low, and in half the number of plants the virus could not be detected. Results of experiments with the monosomic additions indicate, that resistance to P. betae in B. procumbens is located on chromosomes 4 and 8. Some cystosori were present in these addition types, while cystosori were abundantly present in other addition types and all sib-plants. Virus concentrations in the addition types 4 and 8 were lower than in their sib-plants, but in almost all plants the virus could be detected. A significant correlation (r = 0.91; p < 0.05) between average numbers of cystosori and average virus concentrations was found when addition families of type 8 were tested together with B. procumbens and B. vulgaris cv. 'Regina'. [ABSTRACT FROM AUTHOR]

During plant development, the BNYW concentration in several commercially available rhizomania-tolerant sugar beet varieties and one susceptible variety was examined as an index of the intensity of infection. The root weight, sugar content and sugar yield of the same varieties in fields naturally infested with rhizomania were also measured. Significant negative correlations were found between the average virus concentration in the tap root and yield parameters in infested fields. These were largely independent of the growth stage of beet plants used for virological investigations. However, the negative correlations between virus concentration and yield were not significant if rhizomania-tolerant varieties only were compared. The possibility that virus concentration might be used as a criterion for selection in addition to yield performance is discussed. This may lead to selection that is targeted more directly at rhizomania resistance and thereby accelerate breeding work. [ABSTRACT FROM AUTHOR]

Attempts were made to introduce three different isolates of beet necrotic yellow vein virus (BNYW) into the roots of sugarbeets by means of mechanical inoculation. In Chenopodium quinoa these isolates had produced different patterns of viral RNA. The RNA pattern of isolate P was similar to that found in sugarbeets infected naturally by means of the vector Polymyxa betae. RNA 3 and 4 were partially deleted in isolate Y and apparently absent in isolate R. About 20% of the sugarbeet roots inoculated either with isolate P or Y became infected systemically, but with isolate R no systemic infections were recorded. In tap and side roots of plants infected with isolate P the virus concentration remained high for at least ten months and the tap roots of these plants showed a very poor growth. In tap and side roots of plants infected with isolate Y the virus concentration gradually dropped until it reached the limit of detectability. The tap roots of these plants became about five times as big as those infected with isolate P. Our results indicate that B N YW with full length RNA 3 and 4 can cause heavy damage to sugarbeets also in the absence of Polymyxa betae and that RNA 3 and/or 4 -- in addition to a recently suggested involvement in virus transmission by P. betae -- apparently also facilitate the persistent spread of the virus in sugarbeet roots. [ABSTRACT FROM AUTHOR]