Transcriptionally and post-transcriptionally regulated response of 13 calmodulin genes to tobacco mosaic virus-induced cell death and wounding in tobacco plant

2001 ◽  
Vol 268 (14) ◽  
pp. 3916-3929 ◽  
Author(s):  
Hiromoto Yamakawa ◽  
Ichiro Mitsuhara ◽  
Naoko Ito ◽  
Shigemi Seo ◽  
Hiroshi Kamada ◽  
...  
Keyword(s):  
Cell Death ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Tobacco Plant

Effects of homeopathic arsenic on tobacco plant resistance to tobacco mosaic virus.

Homeopathy ◽  
2003 ◽  
Vol 92 (4) ◽  
pp. 195-202 ◽  
Author(s):  
L Betti ◽  
L Lazzarato ◽  
G Trebbi ◽  
M Brizzi ◽  
GL Calzoni ◽  
...  
Keyword(s):  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Plant Resistance ◽  
Tobacco Plant

Pathogen-induced programmed cell death in tobacco

1997 ◽  
Vol 110 (11) ◽  
pp. 1333-1344 ◽  
Author(s):  
R. Mittler ◽  
L. Simon ◽  
E. Lam
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Tobacco Mosaic Virus ◽  
Chloroplast Dna ◽  
Mosaic Virus ◽  
Hypersensitive Response ◽  
Nuclear Periphery ◽  
Death Process ◽  
Tobacco Plants ◽  
Systemic Spread

Sacrificing an infected cell or cells in order to prevent systemic spread of a pathogen appears to be a conserved strategy in both plants and animals. We studied some of the morphological and biochemical events that accompany programmed cell death during the hypersensitive response of tobacco plants infected with tobacco mosaic virus. Certain aspects of this cell death process appeared to be similar to those that take place during apoptosis in animal cells. These included condensation and vacuolization of the cytoplasm and cleavage of nuclear DNA to 50 kb fragments. In contrast, internucleosomal fragmentation, condensation of chromatin at the nuclear periphery and apoptotic bodies were not observed in tobacco plants during tobacco mosaic virus-induced hypersensitive response. A unique aspect of programmed cell death during the hypersensitive response of tobacco to tobacco mosaic virus involved an increase in the amount of monomeric chloroplast DNA. Morphological changes to the chloroplast and cytosol of tobacco cells and increase in monomeric chloroplast DNA occurred prior to gross changes in nuclear morphology and significant chromatin cleavage. Our findings suggest that certain aspects of programmed cell death may have been conserved during the evolution of plants and animals.

scholarly journals NTH201, a Novel Class II KNOTTED1-Like Protein, Facilitates the Cell-to-Cell Movement of Tobacco mosaic virus in Tobacco

2008 ◽  
Vol 21 (5) ◽  
pp. 586-596 ◽  
Author(s):  
Atsushi Yoshii ◽  
Takumi Shimizu ◽  
Akiko Yoshida ◽  
Koji Hamada ◽  
Keitaro Sakurai ◽  
...  
Keyword(s):  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Cultured Cells ◽  
Tobacco Plant ◽  
Cell Movement ◽  
Class Ii ◽  
Early Infection ◽  
Virus Induced Gene Silencing ◽  
Infection Period ◽  
Rna Accumulation

NTH201, a novel class II KNOTTED1-like protein gene, was cloned from tobacco (Nicotiana tabacum cv. Xanthi) and its role in Tobacco mosaic virus (TMV) infection was analyzed. Virus-induced gene silencing of NTH201 caused a delay in viral RNA accumulation as well as virus spread in infected tobacco plants. Overexpression of the gene in a transgenic tobacco plant (N. tabacum cv. Xanthi nc) infected by TMV showed larger local lesions than those of the nontransgenic plant. NTH201 exhibited no intercellular trafficking ability but did exhibit colocalization with movement protein (MP) at the plasmodesmata. When NTH201-overexpressing tobacco BY-2 cultured cells were infected with TMV, the accumulation of MP but not of viral genomic and subgenomic RNA clearly was accelerated compared with those in nontransgenic cells at an early infection period. The formation of virus replication complexes (VRC) also was accelerated in these transgenic cells. Conversely, NTH201-silenced cells showed less MP accumulations and fewer VRC formations than did nontransgenic cells. These results suggested that NTH201 might indirectly facilitate MP accumulation and VRC formation in TMV-infected cells, leading to rapid viral cell-to-cell movement in plants at an early infection stage.

scholarly journals Expression of the Baculovirus p35 Protein in Tobacco Affects Cell Death Progression and Compromises N Gene-Mediated Disease Resistance Response to Tobacco mosaic virus

2003 ◽  
Vol 16 (6) ◽  
pp. 485-494 ◽  
Author(s):  
Olga del Pozo ◽  
Eric Lam
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
N Gene ◽  
Resistance Response ◽  
Tobacco Plants ◽  
Loop Region ◽  
Hr Cell Death

The p35 protein from baculovirus is a broad-range caspase inhibitor and suppresses programmed cell death in animals. We report here the effects of transgenic expression in tobacco of the p35 protein during the hypersensitive response (HR). Expression of p35 causes partial inhibition of nonhost HR triggered by bacteria and gene-for-gene HR triggered by virus. Infection of p35-expressing tobacco plants with Tobacco mosaic virus (TMV) disrupts N-mediated disease resistance, causing systemic spreading of the virus within a resistant background. Mutant variants altered in aspartate residues within the loop region of p35 are inefficient substrates for caspases in vitro, and they do not suppress caspase proteolytic activity in animal systems. Tobacco plants expressing these mutant variants of the p35 protein do not show inhibition of HR cell death or enhanced virus systemic movement. Thus, HR inhibition and TMV systemic spreading phenotype in p35-expressing plants correlate with the ability of the p35 protein to suppress caspase activity in animal systems. In addition, a C-terminal truncated variant of p35 is unable to suppress cell death in animals as well as HR cell death in transgenic tobacco. Our results provide evidence for the participation of caspase-like proteases during the HR. In addition, they suggest that timely activation of cell death is necessary for effective TMV containment within the primary infection site.

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