Hydrogen Peroxide from the Oxidative Burst Is Neither Necessary Nor Sufficient for Hypersensitive Cell Death Induction, Phenylalanine Ammonia Lyase Stimulation, Salicylic Acid Accumulation, or Scopoletin Consumption in Cultured Tobacco Cells Treated with Elicitin

Aquilaria sinensis (Lour.) Gilg produces a highly valuable agarwood characterised by a diverse array of sesquiterpenes and chromone derivatives that can protect wounded trees against potential herbivores and pathogens. A defensive reaction on the part of the plant has been proposed as the key reason for agarwood formation, but the issue of whether programmed cell death (PCD), an important process of plant immune responding, is involved in agarwood formation, still needs to be clarified. In this study, treatment of cultured cell suspensions with hydrogen peroxide (H2O2) induced the production of sesquiterpenes due to endogenous accumulation of salicylic acid (SA) and elevations in the expression of sesquiterpene biosynthetic genes. Moreover, PCD was stimulated by H2O2 in cultured cell suspensions of A. sinensis due to the induction of caspase activity, upregulated expression of metacaspases and cytochrome c, and SA accumulation. Our findings demonstrate for the first time that H2O2 stimulates PCD, SA accumulation and sesquiterpene production in cultured cell suspensions of A. sinensis. Furthermore, results from this study provide a valuable insight into investigations of the potential interactions between sesquiterpene synthesis and PCD during agarwood formation.

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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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Reactive oxygen species promote chloroplast dysfunction and salicylic acid accumulation in fumonisin B1-induced cell death

FEBS Letters ◽

10.1016/j.febslet.2013.05.034 ◽

2013 ◽

Vol 587 (14) ◽

pp. 2164-2172 ◽

Cited By ~ 41

Author(s):

Fuqiang Xing ◽

Zhe Li ◽

Aizhen Sun ◽

Da Xing

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Salicylic Acid ◽

Fumonisin B1 ◽

Reactive Oxygen ◽

Oxygen Species ◽

Acid Accumulation ◽

Salicylic Acid Accumulation

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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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Overexpression of BAK1 causes salicylic acid accumulation and deregulation of cell death control genes

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2017.01.166 ◽

2017 ◽

Vol 484 (4) ◽

pp. 781-786 ◽

Cited By ~ 6

Author(s):

Sun Young Kim ◽

Yun Shang ◽

Se-Hwan Joo ◽

Seong-Ki Kim ◽

Kyoung Hee Nam

Keyword(s):

Cell Death ◽

Salicylic Acid ◽

Acid Accumulation ◽

Salicylic Acid Accumulation

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

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2003.16.12.1145 ◽

2003 ◽

Vol 16 (12) ◽

pp. 1145-1153 ◽

Cited By ~ 34

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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Feedback Control of the Arabidopsis Hypersensitive Response

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.2004.17.4.357 ◽

2004 ◽

Vol 17 (4) ◽

pp. 357-365 ◽

Cited By ~ 13

Author(s):

Chu Zhang ◽

Annie Tang Gutsche ◽

Allan D. Shapiro

Keyword(s):

Hydrogen Peroxide ◽

Salicylic Acid ◽

Pseudomonas Syringae ◽

Hypersensitive Response ◽

Ion Leakage ◽

Wild Type ◽

Regulatory Circuits ◽

Acid Accumulation ◽

Salicylic Acid Accumulation ◽

Hydrogen Peroxide Accumulation

The plant hypersensitive response (HR) to avirulent bacterial pathogens results from programmed cell death of plant cells in the infected region. Ion leakage and changes in signaling components associated with HR progression were measured. These studies compared Arabidopsis mutants affecting feedback loops with wild-type plants, with timepoints taken hourly. In response to Pseudomonas syringae pv. tomato DC3000·avrB, npr1-2 mutant plants showed increased ion leakage relative to wild-type plants. Hydrogen peroxide accumulation was similar to that in wild type, but salicylic acid accumulation was reduced at some timepoints. With DC3000·avrRpt2, similar trends were seen. In response to DC3000·avrB, ndr1-1 mutant plants showed more ion leakage than wild-type or npr1-2 plants. Hydrogen peroxide accumulation was delayed by approximately 1 h and reached half the level seen with wild-type plants. Salicylic acid accumulation was similar to npr1-2 mutant plants. With DC3000·avrRpt2, ndr1-1 mutant plants showed no ion leakage, no hydrogen peroxide accumulation, and minimal salicylic acid accumulation. Results with a ndr1-1 and npr1-2 double mutant were similar to ndr1-1. A model consistent with these data is presented, in which one positive and two negative regulatory circuits control HR progression. Understanding this circuitry will facilitate HR manipulation for enhanced disease resistance.

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Salicylic Acid Accumulation Controlled by LSD1 Is Essential in Triggering Cell Death in Response to Abiotic Stress

Cells ◽

10.3390/cells10040962 ◽

2021 ◽

Vol 10 (4) ◽

pp. 962

Author(s):

Maciej Jerzy Bernacki ◽

Anna Rusaczonek ◽

Weronika Czarnocka ◽

Stanisław Karpiński

Keyword(s):

Cell Death ◽

Salicylic Acid ◽

Abiotic Stress ◽

Wild Type ◽

Pr Genes ◽

Genes Expression ◽

Salicylic Acid Accumulation ◽

Cell Death Phenotype ◽

Insight Into

Salicylic acid (SA) is well known hormonal molecule involved in cell death regulation. In response to a broad range of environmental factors (e.g., high light, UV, pathogens attack), plants accumulate SA, which participates in cell death induction and spread in some foliar cells. LESION SIMULATING DISEASE 1 (LSD1) is one of the best-known cell death regulators in Arabidopsis thaliana. The lsd1 mutant, lacking functional LSD1 protein, accumulates SA and is conditionally susceptible to many biotic and abiotic stresses. In order to get more insight into the role of LSD1-dependent regulation of SA accumulation during cell death, we crossed the lsd1 with the sid2 mutant, caring mutation in ISOCHORISMATE SYNTHASE 1(ICS1) gene and having deregulated SA synthesis, and with plants expressing the bacterial nahG gene and thus decomposing SA to catechol. In response to UV A+B irradiation, the lsd1 mutant exhibited clear cell death phenotype, which was reversed in lsd1/sid2 and lsd1/NahG plants. The expression of PR-genes and the H2O2 content in UV-treated lsd1 were significantly higher when compared with the wild type. In contrast, lsd1/sid2 and lsd1/NahG plants demonstrated comparability with the wild-type level of PR-genes expression and H2O2. Our results demonstrate that SA accumulation is crucial for triggering cell death in lsd1, while the reduction of excessive SA accumulation may lead to a greater tolerance toward abiotic stress.

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