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.

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 Oxidative phosphorylation. The effect of anions on the inhibition by triethyltin of various mitochondrial functions, and the relationship between this inhibition and binding of triethyltin

1972 ◽  
Vol 127 (1) ◽  
pp. 51-59 ◽  
Author(s):  
M. S. Rose ◽  
W. N. Aldridge
Keyword(s):  
Electron Transport ◽  
Oxygen Uptake ◽  
Atp Hydrolysis ◽  
Atp Synthesis ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Hydroxide Ion ◽  
Mitochondrial Functions ◽  
Relationship Of ◽  
The Relationship

1. The binding of triethyltin to rat liver mitochondria is unaffected by the nature of the predominant anion in the incubation medium. 2. With chloride, bromide or iodide as the predominant anion, ATP synthesis linked to the oxidation of pyruvate or succinate and ATP hydrolysis stimulated by 2,4-dinitrophenol are much more sensitive to triethyltin than they are when nitrate or isethionate is the predominant anion. 3. When nitrate or isethionate is the predominant anion, oxygen uptake stimulated by 2,4-dinitrophenol is not inhibited by triethyltin. 4. In the presence of nitrate or isethionate anions, inhibition of ATP synthesis is directly related to the binding of triethyltin to mitochondria. 5. The relationship of the above effects to the anion–hydroxide ion exchange mediated by triethyltin and the relevance of this to published arrangements for coupling of electron transport to ATP synthesis are discussed.

scholarly journals Oxidative Burst Elicited by Bacillus mycoides Isolate Bac J, a Biological Control Agent, Occurs Independently of Hypersensitive Cell Death in Sugar Beet

2003 ◽  
Vol 16 (12) ◽  
pp. 1145-1153 ◽  
Author(s):  
Rebecca L. Bargabus ◽  
Nina K. Zidack ◽  
John E. Sherwood ◽  
Barry J. Jacobsen
Keyword(s):  
Hydrogen Peroxide ◽  
Biological Control ◽  
Cell Death ◽  
Sugar Beet ◽  
Oxidative Burst ◽  
Biological Control Agent ◽  
Control Agent ◽  
Systemic Resistance ◽  
Bacillus Mycoides ◽  
Hypersensitive Cell Death

Response of sugar beet cultivars C40 and USH11 to syringe infiltration of live and dead Bacillus mycoides isolate Bac J, a biological control agent, and virulent and avirulent isolates of Erwinia carotovora pv. betavasculorum was measured by monitoring systemic acquired resistance control of Cercospora beticola, specific activity of chitinase and β-glucanase, the oxidative burst, and hypersensitive cell death at the infiltration site. Priming sugar beet with B. mycoides Bac J (1 × 108 cells/ml) and avirulent isolates of E. carotovora pv. betavasculorum (1 × 106 cells/ml) reduced C. beticola symptoms by nearly 70% on distal, untreated leaves. Systemic resistance responses elicited by live B. mycoides Bac J and avirulent E. carotovora pv. betavasculorum isolates, measured by assays for chitinase and β-glucanase, were statistically equivalent, and biphasic hydrogen peroxide production was observed. Although similar in timing, the second hydrogen peroxide burst was twofold lower for B. mycoides Bac J than for avirulent E. carotovora pv. betavasculorum. Hypersensitive cell death was elicited by aviru-lent E. carotovora pv. betavasculorum but not B. mycoides Bac J. An oxidative burst was elicited by spray-applied B. mycoides Bac J under both light and green light conditions, indicating that the signal produced by B. mycoides Bac J was not reliant on the stomata for entry into sugar beet. A working model for signal delivery and systemic resistance induction by B. mycoides Bac J in sugar beet is proposed.

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