Modifications of the Tobacco Mosaic Virus Coat Protein Gene Affecting Replication, Movement, and Symptomatology

Dawson, William O.; Bubrick, P.; Grantham, George L.

doi:10.1094/phyto-78-783

Cited by 243 publications

(132 citation statements)

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“…On RNA 2, the triple gene block or its gene products are essential for the cell-to-cell spread of the virus (Gilmer et al, 1992). The area of RNA 2 including the coat protein gene was chosen, because for some other viruses and also for BNYVV an involvement of the coat protein in long distance movement and/or symptomatology has been suggested (Dawson et al, 1988;Briddon et al, 1989;Saito et al, 1990;Richards & Tamada, 1992). The four primer pairs described in the Methods section all worked well with cDNA preparations from infected C. quinoa or T. expansa leaves, but with cDNA preparations from sugarbeet tap roots we did not always succeed in obtaining RTPCR products for all four parts of the viral genome.…”

Section: Resultsmentioning

confidence: 99%

Restriction fragment length polymorphism analysis of reverse transcription-PCR products reveals the existence of two major strain groups of beet necrotic yellow vein virus

Kruse¹,

Koenig²,

Hoffmann³

et al. 1994

Journal of General Virology

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Beet necrotic yellow vein virus (BNYVV)-infected sugarbeets were obtained from many parts of Europe and also from some sites in Asia and the U.S.A. Reverse transcription (RT)-PCR products of more than I kbp were obtained for four different regions of the viral genome which may be particularly important with respect to the pathogenic properties of the virus, i.e. for the coat protein and the 42K protein-encoding regions on RNA 2 and for major parts ofRNAs 3 and 4. Restriction fragment length polymorphism (RFLP) patterns obtained with these PCR products revealed the existence of two major strain groups of BNYVV, named type A and type B. The A type was detected in Greece, the former Yugoslavia, Slovakia, parts of Austria, Italy, Spain, parts of France, Belgium, The Netherlands and England as well as in Asia (Turkey, Kazachstan, China and Japan) and the U.S.A. The B type occurs in Germany and parts of France. Mixed infections were detected at the borderline regions between areas of the A and B types. Comparisons of published and newly determined nucleotide sequences of the respective parts of the BNYVV genome indicate that the percentage of nucleotide differences between the A and the B type is approximately 3 % for the respective regions of RNAs 2 and 3 and approximately 1.5 % for RNA 4. Nucleotide sequences appear to be remarkably stable within each of the two strain groups. The majority of the nucleotide differences between the A and B types occur in the third triplet position. The amino acid changes in the coat protein area are outside the four previously determined antigenic regions that are accessible on the surface of the virus particles and are involved in the formation of continuous and presumably also discontinuous epitopes. This may explain why serological differences between the two strain groups have not been found.

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Section: Resultsmentioning

confidence: 99%

Restriction fragment length polymorphism analysis of reverse transcription-PCR products reveals the existence of two major strain groups of beet necrotic yellow vein virus

Kruse¹,

Koenig²,

Hoffmann³

et al. 1994

Journal of General Virology

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“…CSIC.ES al., 1991 ;Taliansky & Garcia-Arenal, 1995) and potexvirus (Chapman et al, 1992) genera. Assembled virions are required for efficient systemic transport of cowpea mosaic virus (CPMV; Wellink & van Kammen, 1989) and tobacco mosaic virus (TMV; Siegel et al, 1962;Dawson et al, 1988;Saito et al, 1990). In the case of tobacco etch potyvirus (TEV), the CP possesses distinct functions required for virion assembly, cell-to-cell movement and long-distance transport (Dolja et al, 1994).…”

Section: Introductionmentioning

confidence: 99%

Long-distance movement of cherry leaf roll virus in infected tobacco plants

Más

Pallás

1996

Journal of General Virology

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The long-distance movement of cherry leaf roll virus (CLRV) in tobacco plants was studied using a tissue printing technique with non-isotopic RNA probes. Time-course analysis revealed that CLRV RNA accumulated in the inoculated leaf at an early stage, such as 20 h post-inoculation. The virus accumulation reached a peak at 8-10 days post-inoculation (d.p.i.) and then progressively decreased. The virus RNA signal was detected before the appearance of symptoms. The virus invaded stem vascular tissues at 3 d.p.i., moving towards the roots before moving to the upper leaves. In systemically infected leaves, the virus appeared first in the basal regions and then moved to the distal parts through the vascular system. The distribution pattern of the virus coat protein in systemically infected leaves was parallel to that observed for the virus RNA, suggesting that CLRV requires the coat protein for long-distance movement. The movement of the virus was influenced by the phyllotactie position of the leaves. The viral symptoms and the virus RNA signal in older systemically infected leaves were asymmetrically distributed, being localized in the side of the lamina closest to the inoculated leaf. Virus distribution in infected plants as well as the susceptibility of the plant to systemic infection were also influenced by the developmental stage of the inoculated leaves. Inoculation of leaves at 95 % of their final size resulted in virus replication but no systemic infection. In fully mature leaves the virus did not replicate.

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“…Collectively, these data suggest that acute chlorosis in wheat infected by WSMV CP deletion mutants is most likely due to degradation of chloroplasts. Mutations in the CP gene of Tobacco mosaic virus (TMV) also elicited acute chlorosis in tobacco (Dawson et al 1988;Lindbeck et al 1992). However, WSMV mutants differ from those of TMV in that WSMV CP deletion mutants formed infectious virions , while TMV CP mutants did not (Dawson et al 1988;Lindbeck et al 1991).…”

Section: Discussionmentioning

confidence: 99%

“…Mutations in the CP gene of Tobacco mosaic virus (TMV) also elicited acute chlorosis in tobacco (Dawson et al 1988;Lindbeck et al 1992). However, WSMV mutants differ from those of TMV in that WSMV CP deletion mutants formed infectious virions , while TMV CP mutants did not (Dawson et al 1988;Lindbeck et al 1991). It has been postulated that virion assembly-deficient CP of TMV mutants forms aggregate-like structures, and these aggregates might have contributed to acute chlorosis (Lindbeck et al 1991(Lindbeck et al , 1992.…”

Section: Discussionmentioning

confidence: 99%

Wheat streak mosaic virus Coat Protein Deletion Mutants Elicit More Severe Symptoms Than Wild-Type Virus in Multiple Cereal Hosts

Satyanarayana

Elowsky

Graybosch

2017

MPMI

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Previously, we reported that coat protein (CP) of Wheat streak mosaic virus (WSMV) (genus Tritimovirus, family Potyviridae) tolerates deletion of amino acids 36 to 84 for efficient systemic infection of wheat. In this study, we demonstrated that WSMV mutants with deletion of CP amino acids 58 to 84 but not of 36 to 57 induced severe chlorotic streaks and spots, followed by acute chlorosis in wheat, maize, barley, and rye compared with mild to moderate chlorotic streaks and mosaic symptoms by wild-type virus. Deletion of CP amino acids 58 to 84 from the WSMV genome accelerated cell-to-cell movement, with increased accumulation of genomic RNAs and CP, compared with the wild-type virus. Microscopic examination of wheat tissues infected by green fluorescent protein–tagged mutants revealed that infection by mutants lacking CP amino acids 58 to 84 caused degradation of chloroplasts, resulting in acute macroscopic chlorosis. The profile of CP-specific proteins was altered in wheat infected by mutants causing acute chlorosis, compared with mutants eliciting wild-type symptoms. All deletion mutants accumulated CP-specific major protein similarly to that in wild-type virus; however, mutants that elicit acute chlorosis failed to accumulate a 31-kDa minor protein compared with wild-type virus or mutants lacking amino acids 36 to 57. Taken together, these data suggest that deletion of CP amino acids 58 to 84 from the WSMV genome enhanced accumulation of CP and genomic RNA, altered CP-specific protein profiles, and caused severe symptom phenotypes in multiple cereal hosts.

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Modifications of the Tobacco Mosaic Virus Coat Protein Gene Affecting Replication, Movement, and Symptomatology

Cited by 243 publications

References 0 publications

Restriction fragment length polymorphism analysis of reverse transcription-PCR products reveals the existence of two major strain groups of beet necrotic yellow vein virus

Restriction fragment length polymorphism analysis of reverse transcription-PCR products reveals the existence of two major strain groups of beet necrotic yellow vein virus

Long-distance movement of cherry leaf roll virus in infected tobacco plants

Wheat streak mosaic virus Coat Protein Deletion Mutants Elicit More Severe Symptoms Than Wild-Type Virus in Multiple Cereal Hosts

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