Phospholipase C/diacylglycerol kinase-mediated signalling is required for benzothiadiazole-induced oxidative burst and hypersensitive cell death in rice suspension-cultured cells

The hypersensitive reaction represents one of the major means by which plants actively defend themselves against infection by pathogenic bacteria, fungi, viruses, and nematodes. This complex defense reaction, often associated with the synthesis of phytoalexins (antimicrobial secondary metabolites), involves at the cellular level highly dynamic cytoplasmic rearrangements, rapid metabolic changes, and finally cell death. It also correlates with the rapid and transient activation of various defense-related genes in a region of tissue surrounding infection sites and later, with the systemic increase in expression of a number of other genes. Examination of the reactions of individual living cells of potato leaves infected with Phytophthora infestans enabled the comprehensive description of the dynamic aspects of all stages of the defense response. Cytochemical investigations, employing cultured cells of parsley infected with P. infestans as a versatile model system, have contributed to a better understanding of cytoplasmic and metabolic processes occurring during the defense response, and suggest that hypersensitive cell death requires the preceding activation of respiration and specific metabolic pathways. Key words: defense responses, defense-related genes, hypersensitive reaction, programmed cell death.

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A signaling pathway, independent of the oxidative burst, that leads to hypersensitive cell death in cultured tobacco cells includes a serine protease

The Plant Journal ◽

10.1046/j.1365-313x.1999.00421.x ◽

1999 ◽

Vol 18 (1) ◽

pp. 105-109 ◽

Cited By ~ 37

Author(s):

Akira Yano ◽

Kaoru Suzuki ◽

Hideaki Shinshi

Keyword(s):

Cell Death ◽

Serine Protease ◽

Signaling Pathway ◽

Oxidative Burst ◽

Hypersensitive Cell Death ◽

Tobacco Cells

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

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2000.13.2.183 ◽

2000 ◽

Vol 13 (2) ◽

pp. 183-190 ◽

Cited By ~ 86

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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