The beet virus Q coat protein readthrough domain is longer than previously reported, with two transmembrane domains

Crutzen, François; Kreit, Marguerite; Bragard, Claude

doi:10.1099/vir.0.008029-0

Cited by 7 publications

(3 citation statements)

References 19 publications

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“…Another hypothesis would involve the intrinsic properties of the BSBV CP-RT, knowing that highly hydrophilic domains containing many charged residues, such as arginine (Hu & Ghabrial, 1995), or the presence of transmembrane motifs (Rath et al, 2009) in proteins might influence their migration on SDS-PAGE. This is supported by the presence in the RT domain of the BSBV CP of two predicted transmembrane helices, as is also reported for the closely related beet virus Q (BVQ) (Crutzen et al, 2009), which would be essential for viral transmission by the vector P. betae (Diao et al, 1999;Adams et al, 2001). Further experiments need to be performed to determine the specificity of CP-RT, from the post-translational modification or intrinsic properties, which influences the molecular mass of the protein on SDS-PAGE.…”

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confidence: 57%

A full-length infectious clone of beet soil-borne virus indicates the dispensability of the RNA-2 for virus survival in planta and symptom expression on Chenopodium quinoa leaves

Crutzen

Mehrvar

Gilmer

et al. 2009

Journal of General Virology

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For a better understanding of the functionality and pathogenicity of beet soil-borne virus (BSBV), full-length cDNA clones have been constructed for the three genomic RNAs. With the aim of assessing their effectiveness and relative contribution to the virus housekeeping functions, transcripts were inoculated on Chenopodium quinoa and Beta macrocarpa leaves using five genome combinations. Both RNAs-1 (putative replicase) and -3 (putative movement proteins) proved to be essential for virus replication in planta and symptom production on C. quinoa, whereas RNA-2 (putative coat protein, CP, and a read-through domain, RT) was not. No symptoms were recorded on B. macrocarpa, but viral RNAs were detected. In both host plants, the 19 kDa CP was detected by Western blotting as well as a 115 kDa protein corresponding to the CP-RT.Beet soil-borne virus (BSBV) is a pomovirus transmitted to Chenopodiaceae by the protist Polymyxa betae (Ivanović et al., 1983), which is also the vector of the aetiological agent of the rhizomania syndrome of sugar beet, beet necrotic yellow vein virus (BNYVV) (Tamada & Baba, 1973). Originally reported in Italy (Canova, 1959), rhizomania disease is now widespread in most countries where sugar beet is grown (McGrann et al., 2009) and BSBV is often found in beet infected with BNYVV (Meunier et al., 2003). However, the pathogenicity of BSBV and its contribution to the rhizomania syndrome remain unclear, with opinions still divided on this (Prillwitz & Schlösser, 1992;Kaufmann et al., 1993;Lindsten, 1993;Rush & Heidel, 1995).The BSBV genome consists of three single-stranded RNAs of positive polarity, packaged into rod-shaped particles (Koenig et al., 1996(Koenig et al., , 1997Koenig & Loss, 1997). RNA-1 (5.8 kb) encodes the putative viral replicase. The 19 kDa coat protein (CP) and a putative 85 kDa read-through (RT) domain are encoded by RNA-2 (3.5 kb). RNA-3 (3.0 kb) comprises three open reading frames (ORFs) encoding three putative proteins (48, 13 and 22 kDa) thought to be responsible for the viral cell-to-cell movement, resembling the well-known triple gene block proteins (TGBs) (Fig. 1).In this study, the contribution of each RNA component to virus survival and symptom expression was investigated through the use of full-length cDNA clones on two host plants, Chenopodium quinoa and Beta macrocarpa. This last plant species was preferred to the natural host Beta vulgaris with a view of developing the basis for further molecular analysis of viral systemicity, following the example of previous studies on BNYVV (Lauber et al., 1998).Full-length cDNA sequences were generated from an Iranian BSBV isolate (Nyshabour, Khorasan Razavi Province), which was trapped from infested soil in roots of B. vulgaris. After total RNA extraction from sugar beet roots using the SV total RNA isolation kit (Promega), the three genomic RNAs were reverse transcribed and amplified by PCR (RT-PCR) using expand reverse transcriptase and the expand long template PCR System (Roche). Primers matching the extremities of the t...

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confidence: 57%

A full-length infectious clone of beet soil-borne virus indicates the dispensability of the RNA-2 for virus survival in planta and symptom expression on Chenopodium quinoa leaves

Crutzen

Mehrvar

Gilmer

et al. 2009

Journal of General Virology

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“…Rhizomania is now widespread in most sugar beet-growing countries (Koenig et al, 2008 ; Chiba et al, 2011 ). Other soil-borne viruses also share the same vector and are frequently found in association with rhizomania: Beet soil-borne virus (BSBV) (Meunier et al, 2003 ), Beet virus Q (BVQ) (Crutzen et al, 2009 ), two viruses belonging to the genus Pomovirus , and Beet soil-borne mosaic virus (BSBMV) (Mahmood and Rush, 1999 ; Ratti et al, 2009 ), another Benyvirus. Beet black scorch virus (BBSV) (Mehrvar and Bragard, 2009 ) was also found associated with sugar beet exhibiting rhizomania symptoms in the USA, Iran and Inner Mongolia of China, but is considered to be transmitted in the soil to host roots by the Chytrid vector Olpidium brassicae (Weiland et al, 2007 ).…”

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confidence: 99%

Long Term Management of Rhizomania Disease—Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields

2018

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Rhizomania disease, caused by the Beet necrotic yellow vein virus (BNYVV), is considered as one of the major constraints for sugar beet production, worldwide. As a result of the introgression of major resistance genes (Holly, Rz2) in commercially available sugar beet varieties, the virus has endured strong selection pressure since the 90s'. Understanding the virus response and diversity to sugar beet resistance is a key factor for a sustainable management of only few resistance genes. Here we report rhizomania surveys conducted in a rhizomania hot spot, the Pithiviers area (France) during a 4-year period and complementary to the study of Schirmer et al. (2005). The study aimed at evaluating the intra- and inter-field BNYVV diversity in response to different sources of resistance and over the growing season. To follow rhizomania development over the sugar beet growing season, extensive field samplings combined with field assays were performed in this study. The evolution of the BNYVV diversity was assessed at intra- and inter-field levels, with sugar beet cultivars containing different resistance genes (Rz1, Rz1 + Heterodera schachtii resistance and Rz1Rz2). Intra-field diversity was analyzed at the beginning and the end of the growing season of each field. From more than one thousand field samples, the simultaneous presence of the different A, B and P types of BNYVV was confirmed, with 21 variants identified at positions 67–70 of the p25 tetrad. The first variant, AYHR, was found most commonly followed by SYHG. Numerous mixed infections (9.93% of the samples), mostly of B-type with P-type, have also been evidenced. Different tetrads associated with the A- or B-type were also found with a fifth RNA-genome component known to allow more aggressiveness to BNYVV on sugar beet roots. Cultivars with Rz1+Rz2 resistant genes showed few root symptoms even if the BNYVV titre was quite high according to the BNYVV type present. The virus infectious potential in the soil at the end of the growing season with such cultivars was also lower despite a wider diversity at the BNYVV RNA3 sequence level. Rz1+Rz2 cultivars also exhibited a lower presence of Beet soil-borne virus (BSBV), a P. betae-transmitted Pomovirus. Cultivars with Rz1 and nematode (N) resistance genes cultivated in field infected with nematodes showed lower BNYVV titre than those with Rz1 or Rz1+Rz2 cultivars. Overall, the population structure of BNYVV in France is shown to be different from that previously evidenced in different world areas. Implications for long-term management of the resistance to rhizomania is discussed.

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“…Several peanut clump virus isolates propagated on N. benthamiana have long deletions in the P39 ORF, but even viruses with deletions could form virions and systemically infect plants (Manohar et al, 1993). For BVQ (genus Pomovirus), it is hypothesized that the coat protein readthrough domain, which has a crucial function in viral transmission by a protist such as Polymyxa, was shortened during serial passage in experimental host plants, Chenopodium quinoa (Crutzen et al, 2009;Koenig et al, 1998). In this study, we determined the sequence of RNA packaged within virions, which was isolated from N. benthamiana leaves after serial passage.…”

Section: Discussionmentioning

confidence: 99%

A novel virus transmitted through pollination causes ring-spot disease on gentian (Gentiana triflora) ovaries

Atsumi

Tomita

Yamashita

et al. 2015

Journal of General Virology

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In this study, we identified a novel virus from gentian (Gentiana triflora) that causes ring-spots on ovaries. Furthermore, the virus causes unusual symptoms, ring-spots that appear specifically on the outer surface of the ovarian wall after pollination. Pollen grains carrying the virus were used to infect host plants by hand-pollination. RNA extracted from purified virions indicated that the virus had two segments, RNA1 and RNA2. The full-length cDNA sequence indicated that RNA1 had two ORFs: ORF1 had methyltransferase and helicase motifs, and ORF2 had an RNA-dependent RNA polymerase motif. RNA2 had five ORFs encoding a coat protein, triple gene block proteins 1-3 and a cysteine-rich protein. The length of RNA1 was 5519 bases and that of RNA2 was 3810 bases not including a polyU/polyA region between the first and second ORFs. Viral RNA does not have a polyA tail at the 39 end. Sequence similarity and phylogenetic analysis suggested that the virus is closely related to members of the genera Pecluvirus and Hordeivirus but distinct from them. These combined results suggest that the causal agent inducing ring-spot symptoms on gentian ovaries is a new virus belonging to the family Virgaviridae but not to any presently known genus. We tentatively name the virus gentian ovary ring-spot virus.

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The beet virus Q coat protein readthrough domain is longer than previously reported, with two transmembrane domains

Cited by 7 publications

References 19 publications

A full-length infectious clone of beet soil-borne virus indicates the dispensability of the RNA-2 for virus survival in planta and symptom expression on Chenopodium quinoa leaves

A full-length infectious clone of beet soil-borne virus indicates the dispensability of the RNA-2 for virus survival in planta and symptom expression on Chenopodium quinoa leaves

Long Term Management of Rhizomania Disease—Insight Into the Changes of the Beet necrotic yellow vein virus RNA-3 Observed Under Resistant and Non-resistant Sugar Beet Fields

A novel virus transmitted through pollination causes ring-spot disease on gentian (Gentiana triflora) ovaries

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