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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.

Beet necrotic yellow vein virus (BNYVV) is causal agent of rhizomania disease, which is the most devastating viral disease in sugar beet production leading to a dramatic reduction in beet yield and sugar content. The virus is transmitted by the ubiquitous distributed soil-borne plasmodiophoromycete Polymyxa betae that infects the root tissue of young sugar beet plants. Rz1 is the major resistance gene widely used in most sugar beet varieties to control BNYVV. The strong selection pressure on the virus population promoted the development of strains that can overcome Rz1 resistance. Resistance-breaking has been associated with mutations in the RNA3-encoded pathogenicity factor P25 at amino acid positions 67–70 (tetrad) as well as with the presence of an additional RNA component (RNA5). However, respective studies investigating the resistance-breaking mechanism by a reverse genetic system are rather scarce. Therefore, we studied Rz1 resistance-breaking in sugar beet using a recently developed infectious clone of BNYVV A-type. A vector free infection system for the inoculation of young sugar beet seedlings was established. This assay allowed a clear separation between a susceptible and a Rz1 resistant genotype by measuring the virus content in lateral roots at 52 dpi. However, mechanical inoculation of sugar beet leaves led to the occurrence of genotype independent local lesions, suggesting that Rz1 mediates a root specific resistance toward BNYVV that is not active in leaves. Mutation analysis demonstrated that different motifs within the P25 tetrad enable increased virus replication in roots of the resistant genotype. The resistance-breaking ability was further confirmed by the visualization of BNYVV in lateral roots and leaves using a fluorescent-labeled complementary DNA clone of RNA2. Apart from that, reassortment experiments evidenced that RNA5 enables Rz1 resistance-breaking independent of the P25 tetrad motif. Finally, we could identify a new resistance-breaking

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De symptomen die de resistentiedoorbrekende varianten van het rhizomanievirus (bijvoorbeeld AYPR) veroorzaken, zijn niet altijd duidelijk te herkennen. Toch kunnen ze aanzienlijke schade veroorzaken aan de financiële opbrengst van de suikerbieten.

In de presentatie worden de symptomen van rhyzomanie besproken. Daarna wordt ingegaan op resistentie doorbrekende tetraden (verspreiding in Nederland). Daarna komen aan de orde: de schade; rassen met aanvullende resistentie tegen rhyzomanie; resistentietoetsen klimaatkamer; resistentietoets klimaatruimte 2012; proefvelden op besmette percelen; resistentietoetsen 2015; de interactie gaat door in het veld; klimaatkamertest diagnostiek monster; advies.

Indeling van de presentatie: Nieuwe ontwikkelingen resistenties bij suikerbieten: 1) rhizoctonia: meer resistentieniveaus. 2) bietencysteaaltjes: opbrengst t.o.v. rhizomanie. 3) aanvullende rhizomanie (rhiz+): wanneer nodig? 4) bladschimmels: verschil tussen rassen? Vervolgens komen aan de orde: Aanbevelende rassenlijst 2016 en regionale cijfers.

Sinds enkele jaren hebben we in Nederland te maken met varianten van het rhizomanievirus die de resistentie van de suikerbietenrassen kunnen doorbreken. De meest gebruikte resistentie tegen rhizomanie (Rz1) is bij deze varianten onvoldoende. Daardoor veroorzaken ze symptomen van rhizomanie en doen (veel) schade.

In de rassenproeven van het KBIVB overheersten de nieuwe dubbelresistente nematodenrassen. Toch blijft het volgens André Wauters interessant om de ontwikkelingen bij de rhizomanierassen in de gaten te houden. Op niet- of zeer weinig besmette percelen is het immers niet nodig om duurder zaad te gebruiken.

Het KBIVB beproefde dit jaar weer bijna evenveel dubbelresistente nematodenrassen als rhizomanierassen. De nematodenrassen blijven vooruitgaan in productiepotentieel, terwijl dit bij de rhizomanierassen enigszins stagneert.

In 2013 zijn er belangrijke verbeteringen te zien in vooral de dubbelresistente rassen. Rassen met resistentie tegen bietencysteaaltjes hebben in de financiële opbrengst een flinke sprong vooruit gemaakt. In alle segmenten komen er nieuwe rassen met aanvullende resistentie tegen varianten van het rhizomanievirus aan. Ook drievoudig resistente rassen die nog in beproeving zijn (tegen rhizomanie, rhizoctonia en bietencysteaaltjes), zijn nu voor het eerst op beperkte schaal verkrijgbaar.

De rhizomanieresistentie is doorbroken. Over heel Nederland komt een nieuwe rhizomanievariant voor. „Breng van je percelen goed in kaart waar je rhizomanie tegenkomt”, adviseert Suiker Unie districtshoofd Peter Koopmans. Want er is inmiddels al een ras met een nieuwe resistentie beschikbaar.

In 2011 is melding gemaakt van een resistentiedoorbrekende variant van het rhizomanievirus. In dit artikel staan de achtergronden, het herkennen en de beheersing ervan.

Powerpointpresentatie van de Suikerbieteninformatiedagen 2012.

In augustus 2011 bracht het IRS naar buiten dat in Nederland een variant van het A-type van het rhizomanievirus aanwezig is, die de resistentie van de huidige rhizomanieresistente rassen kan doorbreken. Dit filmpje laat in een beknopt stappenplan zien hoe bepaald wordt of een suikerbiet dit rhizomanievirus bevat. Als dit zo is, gaan wordt verder gekeken welke variant het betreft. Dit hangt af van de tetrade. Een tetrade is een heel klein stukje van het rhizomanie-eiwit. Afwijkende aminozuren hierin zorgen voor resistentiedoorbraak van het virus.

Powerpointpresentatie van de suikerbieteninformatiedagen 2011. Deze presentatie geeft informatie over de achtergrond van de resistentiedoorbrekende variant van het rhizomanievirus. De kenmerkende symptomen worden getoond. Aangegeven wordt welke typen en varianten het rhizomanievirus kent en waar het in Nederland voorkomt. Het rhizomanievirus komt in heel Nederland voor. De resistentiedoorbrekende variant AYPR is in heel Nederland in grondmonsters aangetroffen en veroorzaakte typische rhizomaniesymptomen in rhizomanieresistenterassen in Flevoland en het zuidwesten. Bemonstering van plekken met en zonder symptomen op hetzelfde perceel geeft aan dat deze variant behoorlijk opbrengst kan kosten. Kenmerkend zijn een lager suikergehalte en een hoger. De resultaten van een veldproef worden behandeld en aangegeven wordt in welke richting gedacht moet worden voor aanvullende resistentie.

De aanbevelende rassenlijst voor 2012 telt drie nieuwe rassen met alleen rhizomanie-resistentie, en twee nieuwe cysteaaltjesresistente rassen.

Rhizomania disease of sugar beet, caused by Beet necrotic yellow vein virus (BNYVV), is responsible for severe economic losses. Due to the widespread occurrence of BNYVV and the absence of other practical and efficient control measures, economic viability of the crop is to the largest extent dependent on the use of varieties genetically resistant to the disease. Recent reports on the emergence of virus strains capable of compromising the Rz1-based resistance as well as on the spread of highly pathogenic RNA 5-containing BNYVV isolates have necessitated a detailed investigation of the situation as it evolves in Greece. The study revealed the widespread occurrence of BNYVV throughout the country as well as the prevalence of pathotype A isolates in all sugar beet growing regions. Sequence determination of the p25 protein, responsible for symptom development, pointed to the amino acid motifs ACHG/VCHG in the hypervariable amino acid region 67-70. However, the presence of valine (V) in position 67 was not associated with increased pathogenicity and resistance breaking properties. Disease severity appeared mostly dependent on agroclimatic conditions influencing the progress of the disease. A survey for a possible occurrence of Beet Soilborne Virus (BSBV) and Beet Virus Q (BVQ) in rhizomania infested fields revealed the co-existence of both viruses, with BVQ being systematically found in co-infections with BNYVV, while BSBV was in all cases only found in triple infections. Towards the exploitation of the antiviral properties of RNA silencing, three intron hairpin constructs carrying parts of the BNYVV replicase gene, were evaluated for their potential to confer rhizomania resistance in Ri T-DNA-transformed sugar beet roots. The results show that transgenic hairy roots were effectively protected against the virus disease and further indicate that the developed methodology for Agrobacterium rhizogenes-mediated transformation can be employed as a suitable platform to study tr

The worldwide extension of the rhizomania disease is one of the most worrying constraints that have to be faced by the sugar beet crop for the past 20 to 30 years. The disease is caused by the Beet necrotic yellow vein virus, a Benyvirus. The virus affects both the quantity and the quality of the production. But the major problem is probably lying in the long-term survival of the virus associated to its vector, Polymyxa betae, a soil-inhabiting plasmodiophoromycete. This vetor has been also shown to transmit other viruses to sugar beet, like the Benyvirus, Beet soil-borne mosaic virus or the Pomovirus like the Beet soil-borne virus and the Beet virus Q. Control of rhizomania depends on the accurate and sensitive detection of BNYVV in plants and soil, for a precocious of infected fields and for breeding resistant sugar beet lines. Also, the complexity introduced by the co-occurrence with other soil-inhabiting viruses raises needs for efficient detection techniques. Therefore, molecular diagnostic methods have been thoroughly used and developed for the identification and quantification of the Beet necrotic yellow vein virus as well as the other soil-borne sugar beet viruses and their vector. A description of sugar beet soil-borne viruses and their vector Polymyxa betae is therefore discussed in this chapter, focusing on the molecular diagnostic methods proposed for their detection and quantification, from serological to the polymerase-based methods.

The worldwide extension of the rhizomania disease is one of the most worrying constraints that have to be faced by the sugar beet crop for he past 20 to 30 years. The disease is caused the Beet necrotic yellow vein virus, a Benyvirus. The virus affects both the quantity and the quality of the production. But the major problem is probably lying in the long-term survival of the virus associated to its vector, Polymyxa betae, a soil-inhabiting plasmodiophoromycete. This vector has been also shown to transmit other viruses to sugar beet, like the Benyvirus Beet soil-borne mosaic virus or the Pomovirus like the Beet soil-borne virus and the Beet virus Q. Control of rhizomania depends on the accurate and sensitive detection of BNYVV in plants and soil, for a precocious of infected fields and for breeding resistant sugar beet lines. Also the complexity introduced by the co-occurrence with other soil-inhabiting viruses raises needs for efficient detection techniques. Therefore, molecular diagnostic methods have been thoroughly used and developed for the identification and quantification of the Beet necrotic yellow vein virus as well as the other soil-borne sugar beet viruses and their vector. A description of sugar beet soil-borne viruses and their vector Polymyxa betae is therefore proposed in this chapter, focusing on the molecular diagnostic methods proposed for their detection and quantification, from serological to the polymerase-based methods.

The production and characterization of monoclonal antibodies (mAbs) to the potato viruses Y and A (PVY and PVA, potyviruses), and to beet necrotic yellow vein virus (BNYVV, a furovirus) are presented. These examples illustrate the value but also some pitfalls of the use of mAbs in virological research. The pitfalls are clearly shown by the studies on PVA and BNYVV. If an incorrect selection procedure was used, mAbs were selected, which reacted only with an epitope of PVA introduced during purification of the virus and which was not present on the virion in situ. Monoclonal antibodies were selected against continuous and discontinuous epitopes to BNYVV. The discontinuous epitopes were easily destroyed by harsh assay conditions. The mAbs to PVY could be used to locate distinct epitopes on the coat protein of the virus. All mAbs proved very helpful in revealing changes in viral epitopes either during purification or after transfer to various host plants.