Interactions Between Tobacco Mosaic Virus, Pokeweed Antiviral Proteins, and Tobacco Cell Wall

1990 ◽  
Vol 80 (7) ◽  
pp. 636 ◽  
Author(s):  
K. Kumon
Keyword(s):  
Cell Wall ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Tobacco Cell ◽  
Antiviral Proteins

scholarly journals Tobacco mosaic virus: a pioneer to cell–to–cell movement

1999 ◽  
Vol 354 (1383) ◽  
pp. 637-643 ◽  
Author(s):  
Vitaly Citovsky
Keyword(s):  
Cell Wall ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Movement Protein ◽  
Cell Movement ◽  
Host Cells ◽  
Specific Cell ◽  
Viral Movement Protein ◽  
Rna Molecules ◽  
Rna Complexes

Cell–to–cell movement of tobacco mosaic virus (TMV) is used to illustrate macromolecular traffic through plant intercellular connections, the plasmodesmata. This transport process is mediated by a specialized viral movement protein, P30. In the initially infected cell, P30 is produced by transcription of a subgenomic RNA derived from the invading virus. Presumably, P30 then associates with a certain proportion of the viral RNA molecules, sequestering them from replication and mediating their transport into neighbouring uninfected host cells. This nucleoprotein complex is targeted to plasmodesmata, possibly via interaction with the host cell cytoskeleton. Prior to passage through a plasmodesma, the plasmodesmal channel is dilated by the movement protein. It is proposed that targeting of P30–TMV RNA complexes to plasmodesmata involves binding to a specific cell wall–associated receptor molecule. In addition, a cell wall–associated protein kinase, phosphorylates P30 at its carboxy–terminus and minimizes P30–induced interference with plasmodesmatal permeability during viral infection.

Ultrastructure of tobacco mosaic virus lesions and surrounding tissue in Phaseolus vulgaris var. Pinto

1971 ◽  
Vol 49 (3) ◽  
pp. 417-421 ◽  
Author(s):  
D. F. Spencer ◽  
W. C. Kimmins
Keyword(s):  
Cell Wall ◽  
Electron Microscope ◽  
Phaseolus Vulgaris ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Healthy Tissue ◽  
Surrounding Tissue ◽  
Infected Area ◽  
Membrane Bound

Leaves of Phaseolus vulgaris var. Pinto were inoculated with the U1 strain of tobacco mosaic virus TMV (U1) and fully expanded lesions and adjacent healthy tissue were examined in the electron microscope. Emphasis was placed on the band of healthy cells (resistant zone) surrounding the lesion, with the object of detecting the first changes in ultrastructure as healthy tissue graded into the infected area. Cells in the resistant zone were characterized by the appearance of membrane-bound vesicular bodies (paramural bodies) between the plasmalemma and cell wall. Where paramural bodies accumulated, the plasmalemma was withdrawn and intercellular cytoplasmic connections through the plasmodesmata were severed. These changes were found most frequently for a distance of about three cell diameters beyond cells visibly infected at the lesion periphery. It is suggested that these changes in ultrastructure are related to the events of localization. Spread of the virus may be inhibited because of a lack of cytoplasmic connections between cells surrounding the virus-induced lesion.

Biochemical changes in cell walls and cellular responses of tobacco leaves related to systemic resistance to blue mold (Peronospora tabacina) induced by tobacco mosaic virus

1992 ◽  
Vol 70 (1) ◽  
pp. 49-57 ◽  
Author(s):  
X. S. Ye ◽  
U. Järlfors ◽  
S. Tuzun ◽  
S. Q. Pan ◽  
J. Kuc
Keyword(s):  
Cell Wall ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Cell Walls ◽  
Induced Systemic Resistance ◽  
Host Cells ◽  
Systemic Resistance ◽  
Blue Mold ◽  
Peronospora Tabacina ◽  
Fungal Hyphae

Inoculation of lower leaves of tobacco cultivar Ky 14, which carries the N gene for resistance to tobacco mosaic virus, with tobacco mosaic virus induced systemic resistance to Peronospora tabacina and a systemic accumulation of cell wall hydroxyproline. Hydroxyproline increased significantly 12 days after induction with tobacco mosaic virus, and more so after challenge with P. tabacina. During this period, hydroxyproline levels in the control plants remained unchanged. Four salt-soluble cell wall proteins were systemically induced. These proteins were not β-1,3-glucanases, chitinases, or hydroxyproline-rich glycoproteins. Light microscopy showed that blue mold development in the induced plants was severely restricted 2 days after challenge; some fungal hyphae were disorganized near the center of infection sites, and adjacent host cells were plasmolyzed and a few collapsed 3 days after challenge. All infection sites in the induced plants were associated with necrotic cells 5–6 days after challenge. Electron microscopy revealed that damage to fungal hyphae, plasmolysis and shrinking of infected cells, and more electron-opaque host cell walls and wall appositions were characteristics of induced resistance. Key words: induced systemic resistance, Nicotiana tabacum, blue mold (Peronospora tabacina).

Plasmodesmata and intercellular transport of viral RNA

2007 ◽  
Vol 35 (1) ◽  
pp. 142-145 ◽  
Author(s):  
C. Hofmann ◽  
A. Sambade ◽  
M. Heinlein
Keyword(s):  
Cell Wall ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Plant Cell Wall ◽  
Movement Protein ◽  
Cell Communication ◽  
Viral Rna ◽  
Intercellular Transport ◽  
Cytoplasmic Bridges ◽  
Spread Of Infection

Cell-to-cell communication in plants involves the symplastic trafficking of informational protein and RNA macromolecules through cytoplasmic bridges in the plant cell wall known as plasmodesmata. Viruses exploit this route for the spread of infection and are used as a model to study the mechanisms by which macromolecules are targeted to the pore. Studies using tobacco mosaic virus have led to the identification of host components that participate in plasmodesmal targeting of viral RNA and movement protein.

Quantitative Measurements on the Ion Etching of TMV

1973 ◽  
Vol 31 ◽  
pp. 336-337
Author(s):  
Irwin Bendet ◽  
Nabil Rizk
Keyword(s):  
Electron Microscope ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Ion Current ◽  
Beam Diameter ◽  
Ion Etching ◽  
Preliminary Results ◽  
Quantitative Measurements ◽  
Monitoring Devices

Preliminary results reported last year on the ion etching of tobacco mosaic virus indicated that the diameter of the virus decreased more rapidly at 10KV than at 5KV, perhaps reaching a constant value before disappearing completely.In order to follow the effects of ion etching on TMV more quantitatively we have designed and built a second apparatus (Fig. 1), which incorporates monitoring devices for measuring ion current and vacuum as well as accelerating voltage. In addition, the beam diameter has been increased to approximately 1 cm., so that ten electron microscope grids can be exposed to the beam simultaneously.

Tobacco Mosaic Virus-Infected Tissue

1985 ◽  
Vol 43 ◽  
pp. 510-511
Author(s):  
Egbert W. Henry
Keyword(s):  
Nicotiana Tabacum ◽  
Tobacco Mosaic Virus ◽  
Chlorogenic Acid ◽  
Mosaic Virus ◽  
Host Resistance ◽  
Oxidative Metabolism ◽  
Leaf Tissue ◽  
Vein Clearing ◽  
Basal Septum ◽  
Concentration Levels

Tobacco mosaic virus (TMV) infection has been studied in several investigations of Nicotiana tabacum leaf tissue. Earlier studies have suggested that TMV infection does not have precise infective selectivity vs. specific types of tissues. Also, such tissue conditions as vein banding, vein clearing, liquification and suberization may result from causes other than direct TMV infection. At the present time, it is thought that the plasmodesmata, ectodesmata and perhaps the plasmodesmata of the basal septum may represent the actual or more precise sites of TMV infection.TMV infection has been implicated in elevated levels of oxidative metabolism; also, TMV infection may have a major role in host resistance vs. concentration levels of phenolic-type enzymes. Therefore, enzymes such as polyphenol oxidase, peroxidase and phenylalamine ammonia-lyase may show an increase in activity in response to TMV infection. It has been reported that TMV infection may cause a decrease in o-dihydric phenols (chlorogenic acid) in some tissues.

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