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).

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.

Acquired systemic resistance to tobacco mosaic virus in Nicotiana tabacum evoked by stem injection with Peronospora tabacina Adam

1963 ◽  
Vol 14 (3) ◽  
pp. 315 ◽  
Author(s):  
M Mandryk
Keyword(s):  
Nicotiana Tabacum ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Systemic Resistance ◽  
Peronospora Tabacina ◽  
Nicotiana Tabacum L ◽  
Stem Injection ◽  
The Difference ◽  
And Control

Resistance to tobacco mosaic virus (TMV) was induced in leaves of Nicotiana tabacum L. (cv. Xanthi and cv. Havana 423) by injecting spore suspensions of Peronospora tabacina Adam into the stems of plants. TMV lesions that developed on the leaves of stem-injected plants were 62% smaller and 32% fewer in number than their counterparts in control plants. While the difference in numbers of lesions on the leaves between injected and control plants decreased from the bottom to the top of the plant, the difference in the size of lesions was maintained at all leaf levels.

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