Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Early events occurring during the hypersensitive resistance response (HR) were examined using the avrRpm1/RPM1 gene-for-gene interaction in Arabidopsis challenged by Pseudomonas syringae pv. tomato. Increases in cytosolic Ca2+ were measured in whole leaves using aequorin-mediated bioluminescence. During the HR a sustained increase in Ca2+ was observed which was dependent on the presence of both a functional RPM1 gene product and delivery of the cognate avirulence gene product AvrRpm1. The sequence-unrelated avirulence gene avrB, which also interacts with RPM1, generated a significantly later but similarly prolonged increase in cytosolic Ca2+. Accumulation of H2O2 at reaction sites, as revealed by electron microscopy, occurred within the same time frame as the changes in cytosolic Ca2+. The NADPH oxidase inhibitor diphenylene iodonium chloride did not affect the calcium signature, but did block H2O2 accumulation and the HR. By contrast, the calcium-channel blocker LaCl3 suppressed the increase in cytosolic Ca2+ as well as H2O2 accumulation and the HR, placing calcium elevation upstream of the oxidative burst.
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PMID:The RPM1 plant disease resistance gene facilitates a rapid and sustained increase in cytosolic calcium that is necessary for the oxidative burst and hypersensitive cell death. 1097 70

Trivalent cations such as those of Al, La, and Gd are phytotoxic. Our previous works showed that addition of LaCl(3) or GdCl(3) to tobacco cells triggers the generation of superoxide (O(2)*-). Here, we show that AlCl(3) at normal physiological pH (5.8) induces much greater production of O(2)*- (detected with a specific chemiluminescence probe), indicating that these trivalent cations similarly induce the oxidative bursts. It was shown that NADPH oxidase is involved in the generation of O(2)*- and the yield of O(2)*- was dose-dependent (ca. 6mM Al, optimal). Following the acute spike of O(2)*-, a gradual increase in cytosolic-free Ca(2+) concentration ([Ca(2+)](c)) was detected with the luminescence of recombinant aequorin over-expressed in the cytosol. Interestingly, a O(2)*- scavenger and a Ca(2+) chelator significantly lowered the level of [Ca(2+)](c) increase, indicating that the Al-induced O(2)*- stimulates the influx of Ca(2+). Compared to the induction of O(2)*- generation, the [Ca(2+)](c) elevation was shown to be maximal (340 nM) at relatively lower Al concentrations (ca. 1.25 mM). Thus, the Al concentration optimal for O(2)*- is too much (inhibitory) for [Ca(2+)](c). In addition, high concentrations of Al were shown to be inhibitory to the H(2)O(2)-induced Ca(2+) influx. This explains the ineffectiveness of high Al concentration in the oxidative burst-mediated induction of [Ca(2+)](c) increase. It is likely that Al-induced [Ca(2+)](c) elevation is manifested from the finely geared balance between the O(2)*- -mediated driving force and the channel inhibition-mediated brake. Furthermore, it is note-worthy that Al (< or =10mM) showed no inhibitory effect on the hypo-osmolarity-induced Ca(2+) influx, implying that Al may be a selective inhibitor of redox-responsive Ca(2+) channels. Possible target channels of Al actions are discussed.
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PMID:Aluminum-induced distortion in calcium signaling involving oxidative bursts and channel regulation in tobacco BY-2 cells. 1289 Apr 76

Responses to oligogalacturonic acid (OGA) were determined in transgenic Arabidopsis thaliana seedlings expressing the calcium reporter protein aequorin. OGA stimulated a rapid, substantial and transient increase in the concentration of cytosolic calcium ([Ca2+]cyt) that peaked after ca. 15 s. This increase was dose-dependent, saturating at ca. 50 ug Gal equiv/ml of OGA. OGA also stimulated a rapid generation of H2O2. A small, rapid increase in H2O2 content was followed by a much larger oxidative burst, with H2O2 content peaking after ca. 60 min and declining thereafter. Induction of the oxidative burst by OGA was also dose-dependent, with a maximum response again being achieved at ca. 50 ug Gal equiv/mL. Inhibitors of calcium fluxes inhibited both increases in [Ca2+]cyt and [H2O2], whereas inhibitors of NADPH oxidase blocked only the oxidative burst. OGA increased strongly the expression of the defence-related genes CHS, GST, PAL and PR-1. This induction was suppressed by inhibitors of calcium flux or NADPH oxidase, indicating that increases in both cytosolic calcium and H2O2 are required for OGA-induced gene expression.
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PMID:Induction of defence gene expression by oligogalacturonic acid requires increases in both cytosolic calcium and hydrogen peroxide in Arabidopsis thaliana. 1522 17

Transgenic Arabidopsis thaliana plants expressing the protein aequorin were used to investigate the transient change in cytosolic calcium ions caused by stimulation through the fungal elicitor Pep-25. Our results show that the elicitor Pep-25 derived from Phytophthora sojae can induce H(2)O(2) production and an increase in cytosolic calcium ions. The transcription of LOX, OPR3, PED, AOS, AOC genes and the protein accumulation of AOS were induced by Pep-25 treatment. Pep-25 also induced an accumulation of jasmonic acid (JA). Blocking the production of H(2)O(2) and the increase of cytosolic calcium ions both suppressed the transcription of LOX, OPR3, PED, AOS, AOC genes, the accumulation of AOS, and the accumulation of JA. These results indicated that the production of H(2)O(2) derived from the plasma-membrane NADPH oxidase and the subsequently increase of cytosolic calcium ions are both required for the activation of the octadecanoid pathway by Pep-25 treatment in A. thaliana.
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PMID:Fungal elicitor Pep-25 increases cytosolic calcium ions, H2O2 production and activates the octadecanoid pathway in Arabidopsis thaliana. 1925 97

Ozone (O(3))-induced cell death in two suspension-cultured cell lines of tobacco (Nicotiana tabacum L.) derived from Bel-W3 (hyper-sensitive to O(3)) and Bel-B (highly tolerant to O(3)) varieties were studied. By exposing the newly prepared cell lines to the pulse of ozonized air, we could reproduce the conditions demonstrating the difference in O(3) sensitivity as observed in their original plants, depending on the exposure time. Since O(3)-induced acute cell death was observed in the dark, the requirement for photochemical reactions could be eliminated. Addition of several ROS scavengers and chelators inhibited the cell death induced by O(3), indicating that singlet oxygen ((1)O(2)), hydrogen peroxide (H(2)O(2)), hydroxyl radical and redox-active metals such as Fe(2+) play central roles in O(3)-induced acute damages to the cells. As expected, we observed the generation of (1)O(2) and H(2)O(2) in the O(3)-treated cells using chemiluminescent probes. On the other hand, an NADPH oxidase inhibitor, superoxide dismutase (SOD), and some SOD mimics showed no inhibitory effect. Thiols added as antioxidants unexpectedly behaved as prooxidants drastically enhancing the O(3)-induced cell death. It is noteworthy that some ROS scavengers effectively rescued the cells from dying even treated after the pulse of O(3) exposure, confirming the post-ozone progress of ROS-dependent cell death mechanism. Since one of the key differences between Bel-B and Bel-W3 was suggested to be the capacity for ROS detoxification by catalase, the endogenous catalase activities were compared in vivo in two cell lines. As expected, catalase activity in Bel-B cells was ca. 7-fold greater than that in Bel-W3 cells. Interestingly, Ca(2+) chelators added prior to (not after) the pulse of O(3) effectively inhibited the induction of cell death. In addition, increases in cytosolic Ca(2+) concentration sensitive to Ca(2+) chelators, ion channel blockers, and ROS scavengers were observed in the transgenic Bel-W3 cells expressing aequorin, suggesting the action of Ca(2+) as a secondary messenger initiating the oxidative cell death. The O(3)-induced calcium response in Bel-W3 cells was much greater than Bel-B cells. Based on the results, possible pathways for O(3)-dependent generation of the lethal level of ROS and corresponding signaling mechanism for induction of cell death were discussed.
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PMID:Ozone-induced cell death mediated with oxidative and calcium signaling pathways in tobacco bel-w3 and bel-B cell suspension cultures. 1951 2