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Rhizomania is the most damaging and widespread disease of the sugar beet crop and is caused by Beet necrotic yellow vein virus vectored by the fungus Polymyxa betae. The only disease management tool used is resistant varieties. In the last 30 years, 'Rizor' and 'Holly' (Rz1) resistances have been the most widely used. Despite the lack of information, a common origin for both types of resistance was hypothesized by some breeders. The aim of this study was to assess the phylogenetic relationship between Rizor and Rz1 by means of SNP analysis. Fifty leaf samples of each were genotyped with a fingerprinting panel of 192 SNPs, using the QuantStudio 12K Flex system coupled with Taqman OpenArray technology. Analysis of molecular variance and principal coordinate analysis confirmed that Rizor and Rz1 cannot be distinguished as separate sources of resistance. [ABSTRACT FROM AUTHOR]

Background: Rhizomania is one of the most devastating diseases of sugar beet. It is caused by Beet necrotic yellow vein virus (BNYVV) transmitted by the obligate root-infecting parasite Polymyxa betae. Beta macrocarpa, a wild beet species widely used as a systemic host in the laboratory, can be rub-inoculated with BNYVV to avoid variation associated with the presence of the vector P. betae. To better understand disease and resistance between beets and BNYVV, we characterized the transcriptome of B. macrocarpa and analyzed global gene expression of B. macrocarpa in response to BNYVV infection using the Illumina sequencing platform. Results: The overall de novo assembly of cDNA sequence data generated 75,917 unigenes, with an average length of 1054 bp. Based on a BLASTX search (E-value ≤ 10−5) against the non-redundant (NR, NCBI) protein, Swiss-Prot, the Gene Ontology (GO), Clusters of Orthologous Groups of proteins (COG) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases, there were 39,372 unigenes annotated. In addition, 4,834 simple sequence repeats (SSRs) were also predicted, which could serve as a foundation for various applications in beet breeding. Furthermore, comparative analysis of the two transcriptomes revealed that 261 genes were differentially expressed in infected compared to control plants, including 128 up- and 133 down-regulated genes. GO analysis showed that the changes in the differently expressed genes were mainly enrichment in response to biotic stimulus and primary metabolic process. Conclusion: Our results not only provide a rich genomic resource for beets, but also benefit research into the molecular mechanisms of beet- BNYV Vinteraction. [ABSTRACT FROM AUTHOR]

Rhizomania, caused by Beet necrotic yellow vein virus (BNYVV), is an important disease affecting sugar beet. Control is achieved through planting of resistant varieties; however, following the introduction of Rz1 , new pathotypes that overcome resistance have appeared. To understand how BNYVV overcomes resistance, we examined quantitative protein differences during compatible and incompatible interactions when sugar beet is infected with either a traditional A-type strain or with an Rz1 resistance breaking strain. Proteomic data suggest distinct biochemical pathways are induced during compatible and incompatible sugar beet interactions with BNYVV. Pathways including the detoxification of reactive oxygen species, UB/proteasome, and photosynthesis should be studied in more depth to characterize roles in symptom development. [ABSTRACT FROM AUTHOR]

Beet necrotic yellow vein virus (BNYVV) is a serious threat to the sugar beet industry worldwide. However, little information is available regarding the genetic diversity and population structure of BNYVV in China. Here, we analyzed multiple sequences from four genomic regions ( CP , RNA3, RNA4 and RNA5) of a set of Chinese isolates. Sequence analyses revealed that several isolates were mixed infections of variants with different genotypes and/or different p25 tetrad motifs. In total, 12 distinct p25 tetrads were found in the Chinese BNYVV population, of which four tetrads were newly identified. Phylogenetic analyses based on four genes ( CP , RNA3- p25 , RNA4- p31 and RNA5- p26 ) in isolates from around the world revealed the existence of two to four groups, which mostly corresponded to previously reported phylogenetic groups. Two new subgroups and a new group were identified from the Chinese isolates in p25 and p26 trees, respectively. Selection pressure analysis indicated that there was a positive selection pressure on the p25 from the Chinese isolates, but the other three proteins were under a negative selection pressure. There was frequent gene flow between geographically distant populations, which meant that BNYVV populations from different provinces were not geographically differentiated. [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]

Beet necrotic yellow vein virus (BNYVV) is a multipartite positive-strand RNA virus. BNYVV RNA-1 encodes a non-structural p237 polyprotein processed in two proteins (p150 and p66) by a cis -acting protease activity. BNYVV non-structural proteins are closely related to replication proteins of positive strand RNA viruses such as hepeviruses rather to other plant virus replicases. The p237 and dsRNA have been localized by TEM in ER structures of infected leaf cells whereas dsRNA was immunolabeled in infected protoplasts. The p150 contains domains with methyltransferase, protease, helicase and two domains of unknown function whereas p66 encompasses the RNA-dependent RNA-polymerase signature. We report the existing interactions between functional domains of the p150 and p66 proteins and the addressing of the benyvirus replicase to the endoplasmic reticulum. Yeast two-hybrid approach, colocalization with FRET-FLIM analyses and co-immunoprecipitation highlighted existing interactions that suggest the presence of a multimeric complex at the vicinity of the cellular membranous web. [ABSTRACT FROM AUTHOR]

The ability of earthwormLumbricus terrestrisL. to suppress the multiplication ofBeet necrotic yellow vein virus(BNYVV) transmitted byPolymyxa betaeand its effects on soil microbial activity were investigated under controlled conditions. BNYVV-infested and a combination of earthworm with BNYVV-infested soil were compared to non-infested soils for their effects on plant and root weights and virus content of two different sugar beet cultivars by using partially resistant (cv. Leila) and susceptible (cv. Arosa) cultivars to the rhizomania disease. Soil testing with sugar beet baiting plants followed by enzyme-linked immunosorbent assay (ELISA) was used to diagnose virus. The results of the statistical analyses showed that total fresh plant and root weights were negatively correlated with BNYVV infection. Addition ofL. terrestrissignificantly enhanced plant and root weights. The earthworm-added soils had higher microbial activity such as basal soil respiration and dehydrogenase activity. The presence of earthworms in the soil did not statistically suppress BNYVV infection (p < 0.05). Sugar beet production may be enhanced by using resistant cultivars with addingL. terrestrisinto soil where rhizomania is present. [ABSTRACT FROM PUBLISHER]

Background Beet necrotic yellow vein virus (BNYVV) is the infectious agent of sugar beet rhizomania, which consists of four or five plus-sense RNAs. RNA4 of BNYVV is not essential for virus propagation in Nicotiana benthamiana but has a major effect on symptom expression. Early reports showed that RNA4-encoded P31 was associated with severe symptoms, such as curling and dwarfing, in N. benthamiana. Results We discovered that the pathogenesis-related protein 10 (PR-10) gene can be up-regulated in BNYVV-infected N. benthamiana in the presence of RNA4 and that it had a close link with symptom development. Our frame-shift, deletion and substitution analysis showed that only the entire P31 could induce PR-10 up-regulation during BNYVV infection and that all the tryptophans and six cysteines (C174, C183, C186, C190, C197 and C199) in the cysteine-rich P31 had significant effects on PR-10 expression. However, P31 could not interact directly with PR-10 in yeast. Conclusions Our data demonstrated that only integrated P31 specifically induced PR-10 transcription, which coincided closely with the appearance of severe symptoms in BNYVV-infected N. benthamiana, although they could not interact directly with each other in yeast. [ABSTRACT FROM AUTHOR]

Viral disease of rhizomania is one of the most important diseases of sugar beet all over the world. The disease significantly has reduced the yield and quality of sugar beet, and has imposed high economic loss to farmers. Long-term breeding programs to introduce tolerant cultivars are the only chance of avoiding further yield losses. This study tried to measure and analyze the growth of shoots and roots of rhizomania-tolerant and -susceptible sugar beet with the aim of providing information for modeling of the rhizomania effects on the growth of sugar beet. Growth indices were used for analyzing, quantification, and time-course of sugar beet growth under infested and non-infested soils conditions. A 2-year experiment was conducted using four sugar beet cultivars in 2010 and 2011 in Mashhad, Iran. The results of this study showed that under infested soils, root dry matter and leaf area index of the susceptible cultivars in comparison to tolerant cultivars were lower by 57 and 24%, respectively. In addition, crop growth rate and net assimilation rate of susceptible cultivars were affected by rhizomania and were lower than in tolerant cultivars. On non-infested soil, the difference between dry matter and growth indices of susceptible and tolerant sugar beet cultivars was not significant. Rhizomania decreased green area and photosynthesis capacity and led to lower growth rate and dry matter production. Our study quantified the growth of rhizomania-infested sugar beet plants in comparison with non-infested plants and provided information to be used for modeling of the rhizomania effects on the growth of sugar beet. [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]

Background: Beet necrotic yellow vein virus (BNYVV), encodes either four or five plus-sense single stranded RNAs and is the causal agent of sugar beet rhizomania disease, which is widely distributed in most regions of the world. BNYVV can also infect Nicotiana benthamiana systemically, and causes severe curling and stunting symptoms in the presence of RNA4 or mild symptoms in the absence of RNA4. Results: Confocal laser scanning microscopy (CLSM) analyses showed that the RNA4-encoded p31 protein fused to the red fluorescent protein (RFP) accumulated mainly in the nuclei of N. benthamiana epidermal cells. This suggested that severe RNA4-induced symptoms might result from p31-dependent modifications of the transcriptome. Therefore, we used next-generation sequencing technologies to analyze the transcriptome profile of N. benthamiana in response to infection with different isolates of BNYVV. Comparisons of the transcriptomes of mock, BN3 (RNAs 1+2+3), and BN34 (RNAs 1+2+3+4) infected plants identified 3,016 differentially expressed transcripts, which provided a list of candidate genes that potentially are elicited in response to virus infection. Our data indicate that modifications in the expression of genes involved in RNA silencing, ubiquitin-proteasome pathway, cellulose synthesis, and metabolism of the plant hormone gibberellin may contribute to the severe symptoms induced by RNA4 from BNYVV. Conclusions: These results expand our understanding of the genetic architecture of N. benthamiana as well as provide valuable clues to identify genes potentially involved in resistance to BNYVV infection. Our global survey of gene expression changes in infected plants reveals new insights into the complicated molecular mechanisms underlying symptom development, and aids research into new strategies to protect crops against viruses. [ABSTRACT FROM AUTHOR]

Sugar beet is one of the most important industrial crops in Iran. For the last two decades it has been mainly affected by a destructive virus, beet necrotic yellow vein virus (BNYVV). The Polymyxa betae is the only natural transmitting agent of the disease among the plants. Developing accurate diagnostic methods may have a major impact on the rising of resistant germplasms. In the present study, specific monoclonal recombinant antibodies in the form of single chain variable fragments (scFv) were obtained from na've phage display libraries. The fungus specific glutathione-S-transferase (GST) protein was chosen as an antigen for developing antibodies and diagnostic purposes. To generate specific scFv, screening of Tomlinson phage display libraries was performed by applying both recombinant and native fungal GST. Using the recombinant GST in the panning process resulted in the isolation of an antibody only bound to recombinant GST but it failed to detect native GST in the infected plants. Alternatively, the process of panning was carried out by applying native fungal GST trapped to immunotubes through specific polyclonal antibody intermediate. The recent approach resulted in the selection of a specific scFv binding to native GST which was able to detect the presence of the fungi within infected plants. To the best of our knowledge, this is the first report on the generation of recombinant antibodies against Polymyxa betae, fungal vector of sugar beet rhizomania disease. [ABSTRACT FROM AUTHOR]

The molecular interactions between Polymyxa betae , the protist vector of sugar beet viruses, beet necrotic yellow vein virus (BNYVV), the causal agent of rhizomania, and Beta vulgaris have not been extensively studied. Here, the transmission of BNYVV to sugar beet by P. betae zoospores was optimized using genetically characterized organisms. Molecular interactions of aviruliferous and viruliferous protist infection on sugar beet were highlighted by transcriptomic analysis. P. betae alone induced limited gene expression changes in sugar beet, as a biotrophic asymptomatic parasite. Most differentially expressed plant genes were down-regulated and included resistance gene analogs and cell wall peroxidases. Several enzymes involved in stress regulation, such as the glutathione- S -transferases, were significantly induced. With BNYVV, the first stages of the P. betae life cycle on sugar beet were accelerated with a faster increase of relative protist DNA level and an earlier appearance of sporangia and sporosori in plants roots. A clear activation of plant defenses and the modulation of genes involved in plant cell wall metabolism were observed. The P. betae transcriptome in the presence of BNYVV revealed induction of genes possibly involved in the switch to the survival stage. The interactions were different depending on the presence or absence of the virus. P. betae alone alleviates plant defense response, playing hide-and-seek with sugar beet and allowing for their mutual development. Conversely, BNYVV manipulates plant defense and promotes the rapid invasion of plant roots by P. betae . This accelerated colonization is accompanied by the development of thick-walled resting spores, supporting the virus survival. [Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.

Extraction of high quality DNA and RNA from soil is a most challenging step to identify soil organisms due to the presence of a variety of inhibitors and microbial nucleases. In this study, we have developed a simple extraction method for simultaneous purification of DNA and RNA from soil. The isolated nucleic acids were of high quality allowing for sensitive detection of the oomycete Polymyxa betae and Beet necrotic yellow vein virus (BNYVV) by nested-PCR. The vector and BNYVV were detected in all infested soils but only the vector was detected in some apparently non-infested soils or fallow fields. The method may help in the management of sugar beet rhizomania. [ABSTRACT FROM AUTHOR]

To study molecular evolutionary characteristics and genetics of beet necrotic yellow vein virus (BNYVV) isolates population from Iran, nucleotide sequences of p25 and coat protein (CP) were determined and the amino acids sequences thus deduced were analyzed using phylogenetic and population genetics methods. A survey of BNYVV in Iran indicated the infection of 288 collected samples out of 392 samples in most beet growing areas and that most of the isolates (92%) were of the A-type and the rest of isolates (8%) were P-type. Our molecular evolutionary analysis showed that CP was highly conserved but allowed to assign all isolates to three distinct groups. Different parts of p25 coding regions were under different evolutionary constraints. The most positive selection was detected at the position 68, the second amino acid of the tetrad motif. Iranian isolates were found to cluster with European isolates into three distinct clusters based on p25 sequences. Population genetics analysis revealed that BNYVV populations have low differentiation (Kt= 3.97145) and low diversity (πT= 0.006, Hd= 0.860) with frequent gene flow indicating lack of phylogeographic structure between populations. [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]

Beet necrotic yellow vein virus (BNYVV) was shown to occur in sugar beets in three of six regions surveyed in Lithuania. Characterizing the coat protein (CP) and p25 genes by RT-PCR and sequencing showed the presence of A and B types of BNYVV isolates. The p25 protein of Lithuanian BNYVV isolates contained a distinct amino acid tetrad (residues 67-70) with AYHR associated with a B type isolate and AHHG with two A type isolates. These sequence features were consistent with phylogenetic grouping of isolates based on CP and p25 gene sequences. This is the first characterization of BNYVV isolates in Lithuania. [ABSTRACT FROM AUTHOR]

The A-type of beet necrotic yellow vein virus (BNYVV) is widely distributed in Europe and is one of the major virus types causing rhizomania disease in sugar beet. The closely related P-type is mainly limited to a small region in France (Pithiviers). Both virus types possess four RNAs (RNA1-4), but the P-type harbours an additional fifth RNA species (RNA5). The P-type is associated with stronger disease symptoms and resistance-breaking of Rz1 , one of the two resistance genes which are used to control BNYVV infection. These characteristics are presumably due to the presence of RNA5, but experimental evidence for this is lacking. We generated the first infectious cDNA clone of BNYVV P-type to study its pathogenicity in sugar beet in comparison to a previously developed A-type clone. Using this tool, we confirmed the pathogenicity of the P-type clone in the experimental host Nicotiana benthamiana and two Beta species, B. macrocarpa and B. vulgaris . Independent of RNA5 , both the A- and the P-type accumulated in lateral roots and reduced the taproot weight of a susceptible sugar beet genotype to a similar extent. In contrast, only the P-type clone was able to accumulate a virus titre in an Rz1 -resistant variety whereas the A-type clone failed to infect this variety. The efficiency of the P-type to overcome Rz1 resistance was strongly associated with the presence of RNA5. Only a double resistant variety, harbouring Rz1 and Rz2, prevented an infection with the P-type. Reassortment experiments between the P- and A-type clones demonstrated that both virus types can exchange whole RNA components without losing the ability to replicate and to move systemically in sugar beet. Although our study highlights the close evolutionary relationship between the two virus types, we were able to demonstrate distinct pathogenicity properties that are attributed to the presence of RNA5 in the P-type.

Rhizomania is the most destructive disease in sugar beet throughout the world. The disease is caused by Beet necrotic yellow vein virus (BNYVV). Polymyxa betae (Keskin) is the only known vector of BNYVV, for transmission of the virus between the plants. Developing molecular diagnostic methods has a major impact on forecasting and epidemiological studies as well as screening sugar beet plants used in resistance breeding programmes. In the present study, quantum dots (QDs) were biofunctionalized with a specific antibody against P. betae. The glutathione-S-transferase protein's (GST) corresponding antibody (anti-GST) was effectively conjugated to Tioglicolicacid-modified Cadmium-Telluride QDs (CdTe-QDs) synthesized in an aqueous solution via electrostatic interaction. The dye (Rhodamine) molecules were attached to the GST. Donor–acceptor complexes (QDs-Ab-GST-Rhodamine) were then formed based on the antigen–antibody interaction. The mutual affinity of the antigen and the antibody brought the CdTeQDs and rhodamine together close enough to allow the resonance dipole–dipole coupling required for fluorescence resonance energy transfer (FRET) to occur. The immunosensor constructed showed a high sensitivity and specificity of 100%, acceptable stability and could be used for real sample detection with consistent results. To the best of our knowledge, this is the first report on designing a nano-based biosensing tool for the detection of plant pathogenic fungi. [ABSTRACT FROM PUBLISHER]

A survey was conducted to determine the distribution of Beet necrotic yellow vein virus (BNYVV), Beet soilborne virus (BSBV), their vector Polymyxa betae and sugar beet cyst nematode (Heterodera schachtii Schm.) (SBN) in sugar beet fields in northern parts of Turkey. A total of 200 soil samples were collected at random from fields in Samsun, Amasya, Tokat, Corum, and Cankiri provinces during 2004 and 2005 growing seasons. The results of ELISA tests showed that BSBV was the most prevailing virus (40.5%), followed by BNYVV (27.5%) in the regions. Of the 200 fields surveyed, 92 samples infested by at least one virus (46%), 55 samples infested by SBN (27.5%) and 161 samples infested by viruliferous or aviruliferous P. betae (80.5%). In the mixed infections, the combination BNYVV and BSBV was the most frequent (15%) followed by aviruliferous P. betae+SBN (8.5%). Also, the number of nematode cysts was significantly lower in BNYVV+P. betae, BSBV+P. betae, BNYVV+BSBV+P. betae and aviruliferous P. betae compared with healthy samples. [ABSTRACT FROM AUTHOR]

Beet necrotic yellow vein virus (BNYVV) causes one of the most economically destructive diseases of sugar beet (Beta vulgaris), rhizoma-nia, which may reduce sugar yield by 80%. This field investigation was conducted to evaluate the interactions between spinach genotypes and different BNYVV strains, and to determine whether BNYVV is transmitted through spinach seeds. Eight commercial spinach cultivars were planted in two BNYVV-infested fields and two control fields in Salinas, CA in 2009. Spinach plants in the BNYVV-infested fields showed disease symptoms of yellow-green or light-green vein clearing, mottling, or yellow-green chlorotic lesions on younger leaves as early as 28 days after planting (four- to six-true leaf stage). Leaves may also become stiff, more crinkled, and necrotic. There was an increase of lateral roots and leaf number but a decrease in leaf weight compared to healthy plants. Infected plants often became stunted, deformed, wilted, and dead. Symptomatic leaves and roots from plants with or without leaf symptoms in BNYVV-infested fields all tested positive for BNYVV by enzyme-linked immunosorbent assay. A more aggressive (resistance-breaking) strain of BNYVV led to higher disease incidence in spinach than in the wild type. BNYVV was not transmitted through spinach seeds. There were significant differences in disease development among cultivars, with disease incidence ranging from 8 to 44%, suggesting that genetic improvement of BNYVV resistance through spinach breeding should be feasible. [ABSTRACT FROM AUTHOR]

The article focuses on a study by S. V. Vinogradova and colleagues regarding the effectiveness of 3'-untranslated region (UTR) of the beet yellow virus genomic RNA and beet necrotic yellow vein virus in RNA silencing induction. It states the use of a procedure for transient coexpression in plants and the development of pB_IBYVsil and pB_IBNYVVsil plasmid constructs. Moreover, it implies the role of double-stranded 3'-UTR in making biotechnology sugar beet plants.

Abstract: Economic viability of a sugar beet crop largely depends on its successful protection against rhizomania, a most devastating disease that causes severe losses in root yield, sucrose content and quality. Rhizomania disease is caused by Beet necrotic yellow vein virus (BNYVV), a virus present in most sugar beet growing regions being vectored by the widely spread soil borne protoctist Polymyxa betae Keskin. The only practical means to control the disease is the use of genetically resistant varieties and, to date, such resistance is mainly based on a dominant gene (Rz1) that when present confers a sufficiently high level of protection against BNYVV. However, the emergence of virus strains capable of compromising the resistance employed in commercial varieties as well as a possible spread of more pathogenic isolates threatens crop''s protection efficiency in the future. All these point to the necessity for exploiting new and more effective genetic sources of rhizomania resistance, both by classical and molecular breeding approaches, a practice that is being pursued by the relevant breeding firms. This article critically reviews the various issues related to the disease and its management and particularly to the ones pertaining to pathogen genetic diversity, types of genetic resistance currently employed, as well as to novel biotechnological approaches aiming at the development of better resisting cultivars. [Copyright &y& Elsevier]

The genome of most Beet necrotic yellow vein virus (BNYVV) isolates is comprised of four RNAs. The ability of certain isolates to overcome Rz1-mediated resistance in sugar beet grown in the United States and Europe is associated with point mutations in the pathogenicity factor P25. When the virus is inoculated mechanically into sugar beet roots at high density, the ability depends on an alanine to valine substitution at P25 position 67. Increased aggressiveness is shown by BNYVV P type isolates, which carry an additional RNA species that encodes a second pathogenicity factor. P26. Direct comparison of aggressive isolates transmitted by the vector, Polymyxa betae, has been impossible due to varying population densities of the vector and other soilborne pathogens that interfere with BNYVV infection. Mechanical root inoculation and subsequent cultivation in soil that carried a virus-free P. betae population was used to load P betae with three BNYVV isolates: a European A type isolate, an American A type isolate, and a P type isolate. Resistance tests demonstrated that changes in viral aggressiveness towards Rz1 cultivars were independent of the vector population. This method can be applied to the study of the synergism of BNYVV with other P. betae-transmitted viruses. [ABSTRACT FROM AUTHOR]

Abstract: Crop yield has to increase to meet the expanding demand for food, feed and bio-energy, caused by world population growth and increasing wealth. Raising sugar yield is also the key to sustaining the profitability of the sugar beet crop. This paper describes the factors that impacted on yield differences between 26 ‘top’ and 26 ‘average’ growers based on four years yield data (2000–2004). In 2006 and 2007, the top growers had 20% higher sugar yields compared to their neighbouring average growers. Heterodera schachtii and Beet necrotic yellow vein virus (BNYVV) were mainly found on clay soils. Top growers on clay soil had significantly lower infestation levels of H. schachtii (4.4x lower, P = 0.008), BNYVV (2.7x lower, P = 0.016) and other foliar symptoms (Pseudomonas, Phoma betae and Verticillium spp. combined) (1.5x lower, P < 0.001), than the average growers, respectively. On sandy soils, infestation levels of Meloidogyne spp. (P = 0.016), Cercospora beticola (P = 0.005) and Erysiphe betae (P = 0.027) were significantly lower (5x, 1.4x and 1.8x, respectively) for the top growers. The top growers on clay or sand sowed 5 and 6 days earlier respectively, and made more fungicide applications and thus used more fungicides than the average growers. Insect pests were not observed at levels damaging for sugar yield: Insecticidal seed treatments provided sufficient control of insect pests. In multiple regression, 35% of the variance in sugar yield on clay soils was explained by H. schachtii and BNYVV infestation levels and by sowing date. On sandy soils, the infestation levels of Heterodera betae and Aphanomyces cochlioides, number of fungicide applications and sowing date explained 71% of the variance in sugar yield. Despite crop protection measures, the calculated yield losses due to pests and diseases for the top growers were 30.2 and 13.1% and for average growers were 37.1 and 16.7% on sandy and clay soils, respectively. Therefore, pest and disease infestation levels partly explained the differences in sugar yield between top and average growers analysed. The skills and knowledge of the grower are important to reducing damage by pests and diseases. Communication of knowledge, obtained by research, towards growers is vital for the long-term raising of yield and increasing of productivity in sugar beet, as well as in other crops. [Copyright &y& Elsevier]

survey was carried out to investigate the current situation concerning rhizomania disease incidence in sugar beet cultivation of Greece. A systematic field evaluation over locations and years revealed a consistent disease severity pattern according to favourable agroclimatic conditions and pointed to the so far effectiveness of the Rz1 gene-based resistance, as no major disease outbreaks were observed. Molecular analyses aiming at the characterization of the type and genetic diversity of the virus further confirmed the widespread occurrence of BNYVV in the country, as evidenced by RT-PCR amplification of all five known genomic molecules and nested-PCR assays. None of the isolates contained an RNA 5, typically found in pathotype P. On the basis of RFLP patterns, all BNYVV isolates analysed were classified as pathotype A. Sequence determination of the full-length RNA 3-encoded p25 protein, responsible for symptom development, revealed amino acid motifs ACHG/VCHG in the hypervariable region aa. The presence of valine in position 67 did not appear associated with increased pathogenicity and resistance breaking properties, as earlier reported. [ABSTRACT FROM AUTHOR]

Background: Beet Necrotic Yellow Vein virus (BNYVV) is a member of the genus Benyvirus causing a worldwide sugar beet disease rhizomania. BNYVV contains four or five plus-sense single stranded RNAs. In altered selective conditions, multipartite RNA viruses of plant are prone to undergoing internal deletions, thus turning into Defective RNAs (D RNAs). Although several D RNAs have been reported in BNYVV infection, the spontaneous internal deletion mutants responsible for severe symptom in systemic host Nicotiana benthamiana (N. benthamiana) are not described so far. Results: Systemic host N. benthamiana was inoculated by Chinese BNYVV isolates. RT-PCR and Northern blot showed that the D RNAs forms of BNYVV RNA3 were present in the systemic infection of the N. benthamiana. Three distinct D-RNA3s, named as D-RNA 3α, D-RNA 3β and D-RNA 3γ, were made into infectious clones. When inoculated on the N. benthamiana, the in vitro transcripts of D forms exhibited more stable than that of wild-type RNA3 in systemic movement. Among the detected mutant, the p25 protein frame-shift mutant (D-RNA3α) induced obvious necrotic lesions on Tetragonia.expansa (T. expansa) and pronounced systemic symptom on the N. benthamiana. The D-RNA3α was further mutated artificially to pre-terminate the downstream N protein, leading to the abolishment of the pathogenicity, indicating the N protein was responsible for the necrotic symptom. Conclusion: Our studies demonstrated the internal deletion mutants of BNYVV-RNA3 were spontaneously generated in the systemic infection on N. benthamiana. The internal deletions didn't affect the efficient replication of D-RNA3s, instead by improving the stability and pathogenicity of RNA3 in the systemic host N. benthamiana. Besides, our results also suggested the downstream N protein of RNA3, but not the upstream p25 protein, may play an important role in the systemic infection on N. benthamiana. [ABSTRACT FROM AUTHOR]

Theoretical models predict that, under restrictive host conditions, virus populations will exhibit greater genetic variability. This virus response has been experimentally demonstrated in a few cases but its relation with a virus's capability to overcome plant resistance is unknown. To explore the genetic host effects on Beet necrotic yellow vein virus (BNYV populations that might be related to resistance durability, a wild-type virus isolate was vector inoculated into partially resistant Rzl, Rz2, and susceptible sugar beet cultivars during a serial planting experiment. Cloning and sequencing a region of the viral RNA-3, involving the pathogenic determinant p25, revealed that virus diversity significantly increased in direct proportion to the strength of host resistance. Thus. whereas virus titers were highest, intermediate, and lowest in susceptible, Rzl, and Rz2 plants, respectively; the average number of nucleotide differences among single-plant populations was 0.8 (+0.1) in susceptible, 1.4 (±0.1) in Rzl, and 2.4 (±0.2) in Rz2 genotypes. A similar relationship between host restriction to BNYVV root accumulation and virus genetic variability was detected in fields of sugar beet where these specific Rzl- and Rz2-mediated resistances have been defeated. [ABSTRACT FROM AUTHOR]