Rhizomania: Hide and Seek of Polymyxa betae and the Beet Necrotic Yellow Vein Virus with Beta vulgaris.

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.

[17th plant virology meeting report]. / Compte rendu des 17es Rencontres de virologie végétale.

RVV Plant virology meeting (January 27-31, 2019, Aussois, France) allows researchers, engineers, technicians, students and post-docs to exchange around oral and poster presentations. These convivial meetings are 30 years old and have a nice future.

[Hit two birds with one stone: the multiple properties of (viral) RNA silencing suppressors]. / D'une pierre deux coups : les multiples caractéristiques des suppresseurs (viraux) de l'interférence par l'ARN.

In any organism, gene expression regulation is provided by multiple factors to maintain a harmonious development of individuals. Discovered in the late 1990s, RNA interference (RNAi) completely remodelled the way in which gene expression regulations were initially apprehended. RNAi provides fine regulation at the cellular level and allows organisms to control their development, maintain their genomic integrity and fight against different stresses like viral infection. Exogenous or endogenous double-stranded RNAs initiate RNAi and are recognized and cleaved by Dicer protein in about 20 nucleotide duplexes small RNAs (sRNAs). One strand of the duplex is loaded into a ribonucleoproteic complex, named RISC (RNA-induced silencing complex), composed of at least one ARGONAUTE protein and a sRNA. Therefore, the expression of any RNA possessing the complementary siRNA sequence of the small RNA will be specifically silenced either at the transcriptional or post-transcriptional level. RNAi plays a prominent role in the defence against viral infection and the last two decades of research have refined our knowledge of proteins involved in this pathway. Many viruses counteract the antiviral action of RNAi through the expression of factors (viral suppressor of RNA silencing [VSR]) that were first identified on virally infected plants. However, in mammals, the antiviral role of RNAi remains controversial. Indeed, viral infections are controlled by the interferon response and the antiviral action of RNAi has not been clearly demonstrated in vivo. In this review, the main modes of defence suppression used by VSR and endogenous RNAi suppressors will be presented. Finally, the role of viral non-coding RNAs (ncRNAs) acting as suppressors of RNAi will be discussed.

Hit two birds with one stone: the multiple properties of (viral) RNA silencing suppressors.

In any organism, gene expression regulation is provided by multiple factors to maintain a harmonious development of individuals. Discovered in the late 1990s, RNA interference (RNAi) completely remodelled the way in which gene expression regulations were initially apprehended. RNAi provides fine regulation at the cellular level and allows organisms to control their development, maintain their genomic integrity and fight against different stresses like viral infection. Exogenous or endogenous double-stranded RNAs initiate RNAi and are recognized and cleaved by Dicer protein in about twenty nucleotide duplexes small RNAs (sRNAs). One strand of the duplex is loaded into a ribonucleoproteic complex, named RISC (RNA induced silencing complex), composed of at least one ARGONAUTE protein and a sRNA. Therefore, the expression of any RNA possessing the complementary siRNA sequence will be specifically silenced either at the transcriptional or post-transcriptional level. RNAi plays a prominent role in the defence against viral infection and the last two decades of research have refined our knowledge of proteins involved in this pathway. Many viruses counteract the antiviral action of RNAi through the expression of factors (VSR, Viral suppressor of RNA silencing) that were first identified on virally infected plants. However, in mammals the antiviral role of RNAi remains controversial. Indeed, viral infections are controlled by the interferon response and the antiviral action of RNAi has not been clearly demonstrated in vivo. In this review, the main modes of defence suppression used by VSR and endogenous RNAi suppressors will be presented. Finally, the role of viral non-coding RNAs (ncRNAs) acting as suppressors of RNAi will be discussed.

ICTV Virus Taxonomy Profile: Benyviridae.

The Benyviridae is a family of multipartite plant viruses with rod-shaped virions. Genomes are segmented and comprised of single-stranded, positive-sense RNAs, each with a 5' m7G cap. Unlike rod-shaped viruses classified in the Virgaviridae family, the genome segments have a 3' polyA tract and there is post-translational cleavage of the viral replicase. The better-known members are transmitted by root-infecting vectors in the Plasmodiphorales family, once described as fungi but now classified as Cercozoa. The family has a single genus. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the taxonomy of Benyviridae, which is available at www.ictv.global/report/benyviridae.

ICTV Virus Taxonomy Profile: Virgaviridae.

The family Virgaviridae is a family of plant viruses with rod-shaped virions, a ssRNA genome with a 3'-terminal tRNA-like structure and a replication protein typical of alpha-like viruses. Differences in the number of genome components, genome organization and the mode of transmission provide the basis for genus demarcation. Tobacco mosaic virus (genus Tobamovirus) was the first virus to be discovered (in 1886); it is present in high concentrations in infected plants, is extremely stable and has been extensively studied. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the taxonomy of the Virgaviridae, which is available at www.ictv.global/report/virgaviridae.

Contributions and lessons learned from virology in contemporary biology.

Virology is a young discipline at the origin of discoveries that revolutionized our vision of biology. Often associated to pathological studies, this science raises more fundamental questions and brings molecular tools required for cellular manipulation. If viruses are considered as our enemies, they are used, sometimes as a last attempt, against multidrug resistant bacteria or to treat cancer.

The benyvirus RNA silencing suppressor is essential for long-distance movement, requires both zinc-finger and NoLS basic residues but not a nucleolar localization for its silencing-suppression activity.

The RNA silencing-suppression properties of Beet necrotic yellow vein virus (BNYVV) and Beet soil-borne mosaic virus (BSBMV) cysteine-rich p14 proteins have been investigated. Suppression of RNA silencing activities were made evident using viral infection of silenced Nicotiana benthamiana 16C, N. benthamiana agroinfiltrated with green fluorescent protein (GFP), and GF-FG hairpin triggers supplemented with viral suppressor of RNA silencing (VSR) constructs or using complementation of a silencing-suppressor-defective BNYVV virus in Chenopodium quinoa. Northern blot analyses of small-interfering RNAs (siRNAs) in agroinfiltration tests revealed reduced amounts of siRNA, especially secondary siRNA, suggesting that benyvirus VSR act downstream of the siRNA production. Using confocal laser-scanning microscopy imaging of infected protoplasts expressing functional p14 protein fused to an enhanced GFP reporter, we showed that benyvirus p14 accumulated in the nucleolus and the cytoplasm independently of other viral factors. Site-directed mutagenesis showed the importance of the nucleolar localization signal embedded in a C4 zinc-finger domain in the VSR function and intrinsic stability of the p14 protein. Conversely, RNA silencing suppression appeared independent of the nucleolar localization of the protein, and a correlation between BNYVV VSR expression and long-distance movement was established.

The P25 pathogenicity factor of Beet necrotic yellow vein virus targets the sugar beet 26S proteasome involved in the induction of a hypersensitive resistance response via interaction with an F-box protein.

P25, a Beet necrotic yellow vein virus (BNYVV) pathogenicity factor, interacts with a sugar beet protein with high homology to Arabidopsis thaliana kelch repeat containing F-box family proteins (FBK) of unknown function in yeast. FBK are members of the Skp1-Cullin-F-box (SCF) complex that mediate protein degradation. Here, we confirm this sugar beet FBK-P25 interaction in vivo and in vitro and provide evidence for in planta interaction and similar subcellular distribution in Nicotiana tabacum leaf cells. P25 even interacts with an FBK from A. thaliana, a BNYVV nonhost. FBK functional classification was possible by demonstrating the interaction with A. thaliana orthologs of Skp1-like (ASK) genes, a member of the SCF E3 ligase. By means of a yeast two-hybrid bridging assay, a direct effect of P25 on SCF-complex formation involving ASK1 protein was demonstrated. FBK transient Agrobacterium tumefaciens-mediated expression in N. benthamiana leaves induced a hypersensitive response. The full-length F-box protein consists of one F-box domain followed by two kelch repeats, which alone were unable to interact with P25 in yeast and did not lead to cell-death induction. The results support the idea that P25 is involved in virus pathogenicity in sugar beet and suggest suppression of resistance response.

Beet necrotic yellow vein virus subgenomic RNA3 is a cleavage product leading to stable non-coding RNA required for long-distance movement.

Beet necrotic yellow vein virus (BNYVV) is a multipartite RNA virus. BNYVV RNA3 does not accumulate in non-host transgenic Arabidopsis thaliana plants when expressed using a 35S promoter. However, a 3'-derivative species has been detected in transgenic plants and in transient expression assays conducted in Nicotiana benthamiana and Beta macrocarpa. The 3'-derivative species is similar to the previously reported subgenomic RNA3 produced during virus infection. 5' RACE revealed that the truncated forms had identical 5' ends. The 5' termini carried the coremin motif also present on BNYVV RNA5, beet soil-borne mosaic virus RNA3 and 4, and cucumber mosaic virus group 2 RNAs. This RNA3 species lacks a m(7)Gppp at the 5' end of the cleavage products, whether expressed transiently or virally. Mutagenesis revealed the importance of the coremin sequence for both long-distance movement and stabilization of the cleavage product in vivo and in vitro. The isolation of various RNA3 5'-end products suggests the existence of a cleavage between nt 212 and 1234 and subsequent exonucleolytic degradation, leading to the accumulation of a non-coding RNA. When RNA3 was incubated in wheatgerm extracts, truncated forms appeared rapidly and their appearance was protein- and divalent ion-dependent.