scholarly journals Slow and Prolonged Activation of the p47 Protein Kinase during Hypersensitive Cell Death in a Culture of Tobacco Cells

1999 ◽  
Vol 119 (4) ◽  
pp. 1465-1472 ◽  
Author(s):  
Kaoru Suzuki ◽  
Akira Yano ◽  
Hideaki Shinshi
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Hypersensitive Cell Death ◽  
Tobacco Cells

scholarly journals Induction of Hypersensitive Cell Death by a Fungal Protein in Cultures of Tobacco Cells

1998 ◽  
Vol 11 (2) ◽  
pp. 115-123 ◽  
Author(s):  
Akira Yano ◽  
Kaoru Suzuki ◽  
Hirofumi Uchimiya ◽  
Hideaki Shinshi
Keyword(s):  
Cell Death ◽  
Specific Interaction ◽  
Trichoderma Viride ◽  
Defense Responses ◽  
Hypersensitive Reaction ◽  
Hypersensitive Cell Death ◽  
Tobacco Cells ◽  
Bright Yellow ◽  
Cell Death Program ◽  
Cellular Signal

Treatment of suspension-cultured tobacco (Nicotiana tabacum cv. Xanthi) cells (line XD6S) with fungal proteinaceous elicitors, namely, xylanase (EC 3.2.1.8) from Trichoderma viride (TvX) and xylanase from T. reesei (TrX), induced shrinkage of the cytoplasm, condensation of the nucleus, and, finally, cell death, which were accompanied by typical defense responses that included an oxidative burst and expression of defense genes. A Ca2+ channel blocker, Gd3+, inhibited the typical response of XD6S cells to TvX, which resembled the hypersensitive reaction (HR). These results suggested that the influx of Ca2+ ions plays an important role as a secondary signal. The HR was not observed in TvX-treated tobacco cells (line BY-2) derived from cv. Bright Yellow 2. This result suggests that key features of cultivar-specific interaction can be observed in cultures of tobacco cells. Xylanase from Bacillus circulans (BcX) and B. subtilis (BsX), which has enzymatic properties similar to those of TvX but an amino acid sequence different from that of TvX, did not induce the HR-like response in XD6S cells. These results suggest that the elicitor action of TvX is not due to its ability to hydrolyze cell walls but requires the TvX-specific recognition factors in plant cells. Thus, TvX-induced cell death was not due to some general toxic effect, but seems to be mediated by the activation of a specific cellular signal-transduction cascade that converges with a pathway that activates the intracellular cell death program.

scholarly journals Harpin-Induced Hypersensitive Cell Death Is Associated with Altered Mitochondrial Functions in Tobacco Cells

2000 ◽  
Vol 13 (2) ◽  
pp. 183-190 ◽  
Author(s):  
Zhixin Xie ◽  
Zhixiang Chen
Keyword(s):  
Cell Death ◽  
Electron Transport ◽  
Oxidative Burst ◽  
Atp Synthesis ◽  
Viral Pathogens ◽  
Hypersensitive Cell Death ◽  
Tobacco Cells ◽  
Mitochondrial Functions ◽  
Diphenylene Iodonium ◽  
Salicyl Hydroxamic Acid

Mitochondria play important roles in animal apoptosis and are implicated in salicylic acid (SA)-induced plant resistance to viral pathogens. In a previous study, we demonstrated that SA induces rapid inhibition of mitochondrial electron transport and oxidative phosphorylation in tobacco cells. In the present study, we report that plant programmed cell death induced during pathogen elicitor-induced hypersensitive response (HR) is also associated with altered mitochondrial functions. Harpin, an HR elicitor produced by Erwinia amylovora, induced inhibition of ATP synthesis in tobacco cell cultures. Inhibition of ATP synthesis occurred almost immediately after incubation with harpin and preceded hypersensitive cell death induced by the elicitor. Diphenylene iodonium, an inhibitor of the oxidative burst, did not block harpin-induced inhibition of ATP synthesis or cell death, suggesting that oxidative burst was not the direct cause for these two harpin-induced processes. Unlike SA, harpin had no significant effect on total respiratory O2 uptake of treated cells. However, respiration of harpin-treated tobacco cells became very sensitive to the alternative oxidase inhibitors salicyl-hydroxamic acid and n-propyl gallate. Thus, harpin treatment resulted in reduced capacity of mitochondrial cytochrome pathway electron transport, which could lead to the observed inhibition of ATP synthesis. Given the recently demonstrated roles of mitochondria in apoptosis, this rapid inhibition of mitochondrial functions may play a role in harpin-induced hypersensitive cell death.

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