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Relevant bibliographies by topics / Turnip mosaic virus

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Academic literature on the topic 'Turnip mosaic virus'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Turnip mosaic virus"

1

Kubelková, D., and J. Špak. "Virus diseases of poppy (Papaver somniferum L.) and some other species of the Papaveraceae family – a review." Plant Protection Science 35, No. 1 (1999): 33–36. http://dx.doi.org/10.17221/9671-pps.

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Opium poppy (Papaver somniferum L.) is described in the literature as a natural host of turnip mosaic virus, bean yellow mosaic virus, beet yellows virus and beet mosaic virus, and experimental host of plum pox virus. P. orientale L., a natural host of beet curly top virus, was successfully infected with turnip mosaic virus and cucumber mosaic virus, and P. dubium L. with turnip mosaic virus. P. rhoeas L. is a natural host of turnip mosaic virus, and artificial host of beet yellows, plum pox and cucumber mosaic viruses. P. nudicaule is reported as a natural host of beet curly top, tomato spotted wilt viruses and turnip mosaic, experimentally it was infected with turnip mosaic virus. Eschscholtzia californica Cham. is described as a natural host of aster yellows phytoplasma, and experimental host of bean yellow mosaic virus. In the Czech Republic, only turnip mosaic virus was reliably identified in naturally infected P. somniferum.

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Wilson, M. A. "Turnip Mosaic Virus in Alabama." Plant Disease 70, no. 9 (1986): 892c. http://dx.doi.org/10.1094/pd-70-892c.

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Shattuck, V. I. "UG1 Turnip Germplasm Possessing Resistance to Turnip Mosaic Virus." HortScience 27, no. 8 (1992): 938–39. http://dx.doi.org/10.21273/hortsci.27.8.938.

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Jenner, Keane, Jones, and Walsh. "Serotypic variation in turnip mosaic virus." Plant Pathology 48, no. 1 (1999): 101–8. http://dx.doi.org/10.1046/j.1365-3059.1999.00309.x.

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Canady, Mary A., Steven B. Larson, John Day, and Alexander McPherson. "Crystal structure of turnip yellow mosaic virus." Nature Structural & Molecular Biology 3, no. 9 (1996): 771–81. http://dx.doi.org/10.1038/nsb0996-771.

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Jenner, C. E., F. Sánchez, K. Tomimura, K. Ohshima, F. Ponz, and J. A. Walsh. "Turnip mosaic virus determinants of virulence for Brassica napus resistance genes." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (2002): S155—S157. http://dx.doi.org/10.17221/10343-pps.

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Dominant resistance genes identified in Brassica napus lines are effective against some, but not all, Turnip mosaic virus<br />(TuMV) isolates. An infectious clone of an isolate (UK 1) was used as the basis of chimeric virus constructions using<br />resistance-breaking mutants and other isolates to identify the virulence determinants for three dominant resistance genes.<br />For the resistance gene TuRB01, the presence of either of two mutations affecting the cylindrical inclusion (CI) protein<br />converted the avirulent UK 1 to a virulent isolate. Acquisition of such mutations had a slight cost to viral fitness in<br />plants lacking the resistance gene. A similar strategy is being used to identify the virulence determinants for two more<br />resistance genes present in another B. napus line.

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Farzadfar, Sh, K. Ohshima, R. Pourrahim, A. R. Golnaraghi, S. Sajedi, and A. Ahoonmanesh. "Reservoir Weed Hosts for Turnip mosaic virus in Iran." Plant Disease 89, no. 3 (2005): 339. http://dx.doi.org/10.1094/pd-89-0339c.

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During the summer of 2003, weed samples of Rapistrum rugosum and Sisymbrium loeselii showing severe mosaic, malformation, and stunting were collected from cauliflower fields in Tehran Province of Iran. Using double-antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) with specific polyclonal antibodies, the samples were tested for the presence of Beet western yellows virus, Cauliflower mosaic virus, Radish mosaic virus, Turnip crinkle virus, Turnip mosaic virus (TuMV) (DSMZ, Braunschweig, Germany), Cucumber mosaic virus, and Tobacco mosaic virus (Sanofi Diagnostics Pasteur, Marnes-La-Coquette, France). Leaf extracts were used for mechanical inoculation and they produced chlorotic local lesions on Chenopodium amaranticolor, necrotic lesions on leaves and shoot apex necrosis on Nicotiana glutinosa, leaf deformation, mosaic, and stunting on Petunia hybrida, and severe mosaic, distortion, and stunting on Brassica rapa. These symptoms were similar to those that were described previously for TuMV (4). ELISA results showed that the original leaf samples and inoculated indicator plants reacted positively with TuMV antibodies, but not with antibodies for any of the other viruses listed above. Also, reverse transcription-polymerase chain reaction of total RNA extracted from the collected leaf samples using the universal primers for potyviruses (3) resulted in the amplification of two fragments of the expected sizes, approximately 700 and 1,700 bp. TuMV, a member of the genus Potyvirus in the family Potyviridae, is transmitted by aphids in a nonpersistent manner (4). This virus is geographically widespread with a wide host range that can infect 318 species in 156 genera of 43 plant families including, Brassicaceae, Chenopodiaceae, Asteraceae, Cucurbitaceae, and Solanaceae (2,4). R. rugosum and S. loeselii, two annual or biennial plants in the Brassicaceae family, were common and widely distributed in the fields surveyed. The presence of TuMV-infected weed hosts in cauliflower fields may impact disease management strategies. TuMV was first observed on stock plants (Matthiola sp.) in Iran (1). To our knowledge, this is the first report of natural occurrence of TuMV on weed hosts in Iran. References: (1) M. Bahar et al. Iran. J. Plant Pathol. 21:11, 1985. (2) J. R. Edwardson and R. G. Christie. The potyvirus group. Fla. Agric. Exp. Stn. Monogr. Ser. No. 16, 1991. (3) A. Gibbs and A. Mackenzie. J. Virol. Methods 63:9, 1997. (4) J. A. Tomlinson. Turnip mosaic virus. No. 8 in: Descriptions of Plant Viruses. CMI/AAB, Surrey, England, 1970.

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Spence, N. J., N. A. Phiri, S. L. Hughes, et al. "Economic impact of Turnip mosaic virus, Cauliflower mosaic virus and Beet mosaic virus in three Kenyan vegetables." Plant Pathology 56, no. 2 (2007): 317–23. http://dx.doi.org/10.1111/j.1365-3059.2006.01498.x.

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Nguyen, Ha Anh, Isabelle Jupin, Philippe Decorse, Stephanie Lau-Truong, Souad Ammar, and Nguyet-Thanh Ha-Duong. "Assembly of gold nanoparticles using turnip yellow mosaic virus as an in-solution SERS sensor." RSC Advances 9, no. 55 (2019): 32296–307. http://dx.doi.org/10.1039/c9ra08015e.

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FUJISAWA, Ichiro. "Aphid transmission of turnip mosaic virus and cucumber mosaic virus. 2. Transmission from virus mixtures." Japanese Journal of Phytopathology 51, no. 5 (1985): 562–68. http://dx.doi.org/10.3186/jjphytopath.51.562.

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Dissertations / Theses on the topic "Turnip mosaic virus"

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陳貽進 and Yi-chun Mark Tan. "Studies on the turnip mosaic virus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1990. http://hub.hku.hk/bib/B31210004.

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Tan, Yi-chun Mark. "Studies on the turnip mosaic virus /." [Hong Kong] : University of Hong Kong, 1990. http://sunzi.lib.hku.hk/hkuto/record.jsp?B12907248.

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Thivierge, Karine. "Host proteins involved in «turnip mosaic virus» life cycle." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86689.

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All viruses are gene poor relative to their host, thus, most steps in virus infection involve interactions between viral components and host factors. Identification of these factors represents one of the major frontiers in current virus research. In this study, protein-protein interaction methodologies were used to find host interactors of Turnip mosaic virus (TuMV) RNA-dependent RNA polymerase (RdRP), VPg-protease (VPg- Pro) and P3 protein.<br>First, eukaryotic elongation factor 1A (eEF1A) was shown to interact with TuMV RdRp and VPg-Pro using tandem affinity purification in Arabidopsis thaliana and/or in vitro assays. Interaction of eEF1A with both viral proteins was shown to take place within 6K-VPg-Pro-induced vesicles. The same vesicles were also shown to contain poly(A)-binding (PABP) and heat shock cognate 70-3 proteins (Hsc70), two previously identified RdRp interactors. To further characterize the content of these vesicles upon TuMV infection, a fluorescently labeled 6K-GFP TuMV infectious clone was constructed and used in confocal microscopy experiments. The inclusion of eEF1A, PABP, Hsc70, eukaryotic initiation factor (iso)4E and VPg-Pro in TuMV-induced vesicles was demonstrated. It is well establish that positive-strand RNA viruses assemble their RNA replication complexes on intracellular membranes, usually in association with vesicle formation. For TuMV, our data suggest that it is the 6K-induced vesicles that house the viral replication complex (VRC). Moreover, the presence of replication and translation elements in these vesicles indicates that both processes might be coupled in TuMV VRC.<br>Secondly, the yeast two-hybrid system was used to identify plant P3-interacting proteins in a cDNA library from A. thaliana. A lipase was recovered from the screen and shown to interact with P3 in vitro. Both proteins were also demonstrated to partially co-localize in the cytoplasm of the cell. Given that lipases play important roles in the plant response to biotic stress, this interaction reinforce the role of TuMV P3 in plant resistance and/or pathogenesis.<br>Les virus ont de petits génomes qui codent pour un nombre limité de protéines et dépendent conséquemment des facteurs de l'hôte pour compléter leur cycle de réplication. Dans ce projet, nous avons utilisé différentes méthodes pour identifier des partenaires protéiques de la polymérase virale à ARN (RdRp), de la VPg-Pro et de la protéine P3 du virus de la mosaïque du navet (TuMV).<br>Premièrement, nous avons trouvé que le facteur eucaryote d'élongation de la traduction 1A (eEF1A) interagit avec la RdRp et la VPg-Pro en utilisant une stratégie de purification en tandem in planta et/ou des essais in vitro. Nous avons montré que ces interactions se produisent en association avec les membranes du réticulum endoplasmique, plus précisément dans les vésicules induites par le polypeptide 6K-VPg-Pro. Nous avons aussi démontré que ces mêmes vésicules contiennent les protéines Hsc70-3 et PABP, deux partenaires connus de la RdRp. Afin de poursuivre la caractérisation du contenu de ces vésicules, nous avons créé un vecteur infectieux du TuMV permettant d'étiqueter les vésicules avec la GFP et d'être utilisé en microscopie confocale. À l'aide de ce vecteur, nous avons observé la présence du facteur eEF1a, de la PABP, de la Hsc70, du facteur eucaryote d'initiation de la traduction (iso) 4E et de la VPg-Pro dans les vésicules induites par le TuMV. Il est bien établit que le complexe de réplication des virus à ARN positif est associé aux membranes cytoplasmiques, généralement sous forme de vésicules. Pour le TuMV, nos données semblent indiquer que les vésicules induites par la protéine 6K contiennent le complexe de réplication viral (VRC). De plus, la présence d'éléments participants à la réplication ainsi qu'à la traduction dans ces vésicules suggère que ces deux processus sont possiblement couplés dans le VRC du TuMV.<br>Deuxièmement, le système du double-hybride en levure a été utilisé pour rechercher des partenaires protéiques de P3. Le criblage de P3 contre une banque d'ADNc d'Arabidopsis thaliana a révélé une interaction entre P3 et une lipase. Lorsque exprimées ensembles dans Nicotiana benthamiana, les deux protéines co-localisent au cytoplasme. Étant donné le rôle des lipases dans les réponses des plantes aux attaques pathogènes, cette interaction renforce le rôle suggéré de la protéine P3 dans la pathogenèse et les mécanismes de résistance des plantes.

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Cotton, Sophie. "Characterization and movement of turnip mosaic virus replication complexes." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=86558.

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Viruses are intracellular pathogens that use the host cell to produce new infectious progeny. For all positive-strand RNA viruses that have been investigated so far, viral replication takes place in cytoplasmic virus-induced membrane structures. For turnip mosaic virus (TuMV), the generation of vesicles likely associated with the replication complex depends on the synthesis of the viral protein 6K. To further characterize the vesicles formed during TuMV infection, Nicotiana benthamiana plants were agroinfiltrated with a TuMV infectious clone expressing 6K protein fused to GFP. Using confocal microscopy, cytoplasmic aggregates were observed, corresponding to the 6KGFP-induced vesicles which house the viral replication complexes (VRCs). Intracellular movement of these vesicles was visualized by time-lapse imaging. Vesicle trafficking was inhibited when plants were infiltrated with latrunculin B, an inhibitor of microfilament polymerization. The absence of movement had severe effects on viral accumulation. Viral vesicles also aligned with actin filaments. These results indicate that microfilaments are necessary for VRC trafficking which is important for virus infectivity.<br>The biogenesis of viral vesicles was investigated by infecting cells with two recombinant TuMVs producing 6KGFP or 6KmCherry-labelled vesicles. Individual vesicle within a cell contained unique protein products derived from each recombinant demonstrating the origin of a vesicle from a single viral genome. Green and red sectoring was also observed, meaning that vesicles could fuse together. The presence of the eukaryotic translation factors eIF(iso)4E, PABP and eEF1A enclosed in VRC was demonstrated previously by our group. These data combined to a single-genome origin suggest that viral translation occur within these structures. The same host factors were also found to co-localize with the active replicating sites along with viral proteins VPg-Pro, RdRp and CI using immunofluorescence labelling in infected protoplasts. These data bring accumulating evidence for the possible coupling of viral translation and replication.<br>Les virus sont des parasites intracellulaires qui utilisent la cellule hôte pour produire une nouvelle descendance infectieuse. Pour tous les virus à ARN positif étudiés jusqu'à maintenant, la réplication virale prend place dans des structures membranaires induites par le virus. Chez le virus de la mosaïque du navet (TuMV), la formation de vésicules probablement associées au complexe de réplication dépend de la synthèse de la protéine virale 6K. Afin de caractériser les vésicules formées durant l'infection de TuMV, des plants de Nicotiana benthamiana ont été agroinfiltrés avec un clone infectieux de TuMV exprimant la protéine 6K fusionnée à GFP. Des agrégats cytoplasmiques ont été observés par microscopie confocale, correspondant aux vésicules induites par la protéine 6KGFP et abritant le complexe de réplication virale (VRC). Le mouvement intracellulaire de ces vésicules a été visualisé par imagerie time-lapse. Le trafic des vésicules a été inhibé lorsque les plantes étaient infiltrées avec de la latrunculin B, un inhibiteur de polymérisation des microfilaments. L'absence de mouvement a également conduit à une sévère diminution de l'accumulation virale. Les vésicules colocalisent avec les filaments d'actine. Ces résultats indiquent que les microfilaments sont nécessaires au mouvement des vésicules lequel est important pour l'infection virale.<br>La biogenèse des vésicules virales a été investiguée en infectant les cellules avec deux clones infectieux de TuMV produisant des vésicules étiquetées par 6KGFP ou 6KmCherry. Des vésicules individuelles contenant des protéines uniques dérivant d'un seul clone recombinant a démontré que l'origine des vésicules provient d'un seul génome. Des vésicules ayant des secteurs vert et rouge ont aussi été observé, indiquant que la fusion de vésicules est possible. La présence des facteurs eucaryotes de traduction eIF(iso)4E, PABP et eEF1A à l'intérieur des vésicules a été démontré par notre groupe. Ces données combinées à l'origine unique des vésicules suggèrent que la traduction virale se produit à l'intérieur de ces vésicules. Les mêmes facteurs de traduction ainsi que les protéines virales VPg-Pro, RdRp et CI colocalisent avec les sites de réplication active dans des protoplastes infectés. Ces données apportent des indices supplémentaires sur la possibilité de couplage entre la traduction et la réplication virale chez TuMV.

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Thivierge, Karine. "Protein-protein interactions in turnip mosaic potyvirus replication complex." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80886.

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Interactions between plant and virus proteins play pivotal roles in many processes during the viral infection cycle. Analysis of protein-protein interactions is crucial for understanding virus and host protein functions and the molecular mechanisms underlying viral infection. Several interactions between virus-encoded proteins have been reported. However, few interactions between viral and plant proteins have been identified so far. To examine interactions between Turnip mosaic potyvirus (TuMV) proteins and plant proteins, recombinant proteins were produced and used in ELISA-type assays and in in vitro co-immunoprecipitation experiments. An interaction between TuMV P1 proteinase and wheat poly(A)-binding protein (PABP) was identified. An interaction between P1 protein and the plant Arabidopsis thaliana eukaryotic initiation factor (iso)4E [eIF(iso)4E] was also found. Finally, potential interactions between both TuMV CI and P1 proteins and between TuMV CI protein and eIF(iso)4E were identified.

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Syme, Jennifer. "Characterization of Arabidopsis thaliana (Columbia) infected with turnip mosaic virus (TuMV)." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=24043.

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The response of Arabidopsis thaliana (Columbia) to infection with turnip mosaic virus (TuMV) was characterized at the level of: disease symptom expression, cell content and protein composition. Visual symptoms observed were chlorotic and mottled leaf colouring, severely stunted growth, distortion of leaf blades and delayed bolting. All plants died before seed cases dehisced. Electron microscopy revealed three types of cylindrical inclusion bodies: pinwheels, scrolls and laminated aggregates, in the cytoplasm of infected plants similar to those observed in other plants infected with TuMV. Inoculation of Arabidopsis with TuMV resulted in quantitative changes in several proteins in both soluble and membrane proteins, as revealed by electrophoresis on 12% polyacrylamide gels. Antibodies were made to both infected membrane and soluble proteins. Western blots of infected and uninfected, soluble and membrane proteins probed with antibodies revealed quantitative changes in the same proteins identified by polyacrylamide gels. A CNBr 4B activated sepharose column was used to make infection-specific antibodies to infected soluble proteins. No infection-specific host proteins were detected in Arabidopsis infected with TuMV.

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Yang, Chunling. "Functional Genomic analysis of Turnip mosaic virus infection in Arabidopsis thaliana." [Ames, Iowa : Iowa State University], 2007.

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Hughes, Sara Louise. "Interaction of turnip mosaic virus (TuMV) with members of the Brassicaceae." Thesis, University of Birmingham, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401328.

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Rushholme, Rachel L. "The genetic control of resistance to turnip mosaic virus (TuMV) in Brassica." Thesis, University of East Anglia, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327536.

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Berthelot, Edwige. "Etude de l'activation de la transmission du Turnip mosaic virus par pucerons." Thesis, Montpellier, SupAgro, 2018. http://www.theses.fr/2018NSAM0039.

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Beaucoup de virus de plante sont transmis selon le mode non-circulant par vecteurs hémiptères, souvent des pucerons. Ce mode de propagation répand les virus très rapidement d’un hôte à l’autre, ce qui cause d’innombrables dégâts sur de nombreuses cultures d'intérêt agronomique. Actuellement, le manque de connaissances sur leur processus de transmission constitue un frein pour le développement de méthodes de lutte efficaces. Récemment, des résultats ont montré qu’un virus modèle, le Cauliflower mosaic virus (CaMV, genre Caulimovirus), répond à l'arrivée de son vecteur puceron en formant, à ce moment précis et de manière réversible, des complexes transmissibles du virus, obligatoire pour son acquisition par le puceron. Ce phénomène extraordinaire nommé « activation de la transmission (AT) » contrôle l’acquisition du virus et donc sa transmission. Il constitue une découverte majeure pour la transmission non-circulante et ouvre de nombreuses perspectives de recherche dont celle d’élargir ce phénomène à autres virus pour savoir si l’AT est un phénomène généralisé dans la propagation des virus.Dans cette optique, nous nous sommes intéressés à un virus non apparenté au CaMV, le Turnip mosaic virus (TuMV), un Potyvirus, également transmis par pucerons. La transmission du TuMV dépend de l’interaction directe de la particule virale et de la protéine virale facteur assistant de la transmission (HC-Pro). En effet, HC-Pro doit former avec la particule un complexe transmissible, seule forme du virus pouvant être acquis par le vecteur. Nos résultats montrent que le TuMV utilise l’AT et qu’elle est dépendante de la présence d’espèces réactives de l’oxygène (ROS) et de la signalisation calcique. L’AT du TuMV est corrélée avec la formation d’oligomères par ponts disulfures de HC-Pro et avec la formation des complexes transmissibles HC-Pro/particules virales dans les cellules végétales. Notre analyse pharmacologique a montré que l’AT du CaMV dépendait également de la présence des ROS et de la signalisation calcique. Ces deux voies de signalisation sont donc impliquées dans les étapes présumées précoces de l’AT du CaMV et du TuMV. Des expériences avec d’autres composés ont mis en évidence que les étapes suivantes de l’AT sont différentes pour les deux virus. Une recherche d’éliciteurs de l’AT a été initiée mais n’a pour l’instant pas permis d’en identifier un.Ces résultats ont mis en évidence l’existence de l’AT pour un deuxième genre de virus non-circulant, suggérant qu’il pourrait s’agir d’un mode de transmission général. Ces nouvelles données ouvrent, d’un point de vu appliqué, de nouvelles perspectives pour les stratégies de lutte, visant à interrompre spécifiquement le processus de l’AT<br>Many plant viruses are transmitted in non-circulative manner by hemipteran vectors, often aphids. This transmission mode spreads viruses very quickly from one host to another and thereby causes countless damage on many crops of agronomic interest. Currently, the lack of knowledge about their transmission process is a hindrance to the development of effective control methods. Recently, results have shown that the model virus, Cauliflower mosaic virus (CaMV, genus Caulimovirus), responds to the arrival of aphid vectors by forming, at this time and reversibly, virus transmissible complexes, obligatory for the acquisition by the aphid. This extraordinary phenomenon called "transmission activation (TA)" controls the virus acquisition and thus its transmission. It’s a major discovery in non-circulative transmission and opens many research perspectives including expanding this phenomenon to other viruses to see if TA is a widespread phenomenon in the viruses propagation.Having this in mind, we are interested to study a virus unrelated to CaMV, Turnip mosaic virus (TuMV), a Potyvirus, also transmitted by aphids. The TuMV transmission depends on the direct interaction of the virus particle and the viral helper component protease (HC-Pro). Indeed, HC-Pro must form with the virus particle a transmissible complex, the only form of virus that can be acquired by the vector. Our results show that TuMV uses TA and that its TA depends on the presence of reactive oxygen species (ROS) and on calcium signaling. TuMV TA is correlated with the formation of HC-Pro disulfide bond mediated oligomers and the formation of HC-Pro transmissible complexes HC-Pro / viral particle in plant cells. Our pharmacological analysis showed that CaMV TA also depends on the presence of ROS and calcium signaling. These two signaling pathways are therefore involved presumably in the early stages of CaMV and TuMV TA. Experiments with other compounds have shown that the following steps of TA are different for the two viruses. A search for elicitors of the TA has been initiated but has not been successful yet.These results provide evidence of the existence of TA for a second genus of non-circulative virus, suggesting that this might be a general transmission mode. These new data open, from an applied point of view, new perspectives for control strategies, aimed at specifically interrupting the TA process

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Books on the topic "Turnip mosaic virus"

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Ontario. Ministry of Agriculture and Food. Turnip mosaic virus (tumv) of rutabaga. s.n, 1988.

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Weiland, John J. The roles of turnip yellow mosaic virus genes in virus replication. 1992.

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Tsai, Ching-Hsiu. Characterization of the role of the 3' noncoding region of turnip yellow mosaic virus RNA. 1993.

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Bransom, Kathryn L. Gene expression of proteins involved in replication of turnip yellow mosaic virus. 1994.

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Wallace, S. Ellen. Search for protein-protein interactions underlying the cis-preferential replication of turnip yellow mosaic virus. 1997.

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Wallace, S. Ellen. Search for protein-protein interactions underlying the cis-preferential replication of turnip yellow mosaic virus. 1997.

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Book chapters on the topic "Turnip mosaic virus"

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Shattuck, V. I. "The Biology, Epidemiology, and Control of Turnip Mosaic Virus." In Horticultural Reviews. John Wiley & Sons, Inc., 2010. http://dx.doi.org/10.1002/9780470650523.ch4.

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Trusov, Yuri, Ralf G. Dietzgen, Natsumi Maruta, and Jose R. Botella. "Simplified Assays for Evaluation of Resistance to Alternaria brassicicola and Turnip Mosaic Virus." In Plant Signal Transduction. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3115-6_18.

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Ebel, Jean-Pierre, Richard Giegé, and Catherine Florentz. "Structural and Functional tRNA Mimicry of the 3’-end of Turnip Yellow Mosaic Virus RNA." In Evolutionary Tinkering in Gene Expression. Springer US, 1989. http://dx.doi.org/10.1007/978-1-4684-5664-6_3.

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Dreher, T. W., and J. J. Weiland. "Preferential replication of defective turnip yellow mosaic virus RNAs that express the 150-kDa protein in cis." In Positive-Strand RNA Viruses. Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9326-6_19.

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Castells-Graells, Roger, George P. Lomonossoff, and Keith Saunders. "Production of Mosaic Turnip Crinkle Virus-Like Particles Derived by Coinfiltration of Wild-Type and Modified Forms of Virus Coat Protein in Plants." In Methods in Molecular Biology. Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7808-3_1.

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Séron, Karin, Françoise Bernardi, Gabrièle Drugeon, and Anne-Lise Haenni. "Strategies of Expression of Turnip Yellow Mosaic Virus in Vivo: Developmental Approach for the Study of the Autocatalytic Cleavage of the 206k Polyprotein." In Developments in Plant Pathology. Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1737-1_31.

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Conference papers on the topic "Turnip mosaic virus"

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Wu, Chia-Che, Ping-Kuo Tseng, Meng-Jhu Hou, and Ching-Hsiu Tsai. "Adhesive Density of 11-Mercaptoundecanoic Acid (MUA) and Turnip Yellow Mosaic Virus (TYMV) in Microfluidic Channels." In ASME 2009 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2009. http://dx.doi.org/10.1115/detc2009-86222.

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Abstract:

Recently, there has been an increasing interest to develop rapid, reliable and low-concentration detection methods of micro-organisms involved in bioterrorism, food poisoning, and clinical problems. How to detect virus at concentration below the threshold will be challenging with respect to specificity, selectivity, and sensitivity. Among all parameters, sensitivity is probably the most critical consideration. If the sensitivity is not satisfied for real-time detection, researchers need to duplicate numerous numbers of viruses. However, it will substantially increase processing times and experimental hazard. To increase the sensitivity of virus sensors, this paper discusses how to increase the density of linkers and viruses on sensor’s surface in the microfluidic channels. In the future, researcher could use emerging technology, such as PT-PCR, QCM, C-V and I-V measurements, etc, to detect viruses on sensor’s surface. Usually microorganisms, molecules, or viruses in the fluidic environment are at very low Reynolds numbers because of tiny diameters. At very low Reynolds numbers, viscous forces of molecules and viruses will dominate. Those micro- or nanoparticles will stop moving immediately when flows cease and drag forces disappear. Of course, molecules and viruses are still subject to Brownian motion and move randomly. In order to increase the adhesion density of micro- and nanoparticles on sensor’s surface, designs of the flow movements in microfluidic channel is proposed. Adhesion density of linker 11-mercaptoundecanoic acid (MUA) and turnip yellow mosaic virus (TYMV) with specific quantum dots were measured by confocal microscope. Results show that TYMV and MUA layers disperse randomly by dipping method. Infusion rate, flow rate, and transverse flow could affect the adhesion densities of recognition layers on sensors’ surface. Adhesion densities of MUA and TYMV can be reached 70∼80% by microfluidic method to contrast just 10% by dipping method.

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2

Zhao, Shuang, and Xufeng Hao. "High Level Resistance to TuMV (Turnip Mosaic Virus) in Transgenic Mustard with the Antisense NIb Gene of the Virus." In 2010 International Conference on Computational and Information Sciences (ICCIS). IEEE, 2010. http://dx.doi.org/10.1109/iccis.2010.267.

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3

Wu, Chia-Che, Ping-Kuo Tseng, and Ching-Hsiu Tsai. "Improving Adhesion Density and Coverage Uniformity of Antibody-Antigen Binding on a Sensor Surface Using U-Type, T-Type and W-Type Microfluidic Devices." In ASME 2011 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. ASMEDC, 2011. http://dx.doi.org/10.1115/detc2011-47528.

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Abstract:

Usually microorganisms, molecules, or viruses in the fluidic environment are at very low Reynolds numbers because of tiny diameters. At very low Reynolds numbers, viscous forces of molecules and viruses will dominate. Those micro- or nanoparticles will stop moving immediately when flows cease and drag forces disappear, those phenomena were discovered by the fluorescent particle experiment. Of course, molecules and viruses are still subject to Brownian motion and move randomly. In order to increase the adhesion density of micro- and nanoparticles on sensor’s surface, designs of the flow movements in microfluidic channel is proposed. Adhesion density of linker 11-mercaptoundecanoic acid (MUA) and Turnip yellow mosaic virus (TYMV) with specific quantum dots were measured by confocal microscope. Fluorescent intensity and coverage of quantum dots are used to identify the adhesion density quantitatively. Results show that TYMV and MUA layers disperse randomly by dipping method. Fluorescent intensity of quantum dots; i.e. relative to the amount of MUA and TYMV; were 2.67A.U. and 19.13A.U., respectively, in W-type microfluidic devices to contrast just 1.00A.U. and 1.00A.U., respectively, by dipping method. Coverage of MUA and TYMV were 80∼90% and 70∼90%, respectively, in W-type microfluidic channel to contrast just 20∼50% and 0∼10%, respectively, by dipping method.

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