Activation of the oxidative burst in aequorin-transformed Nicotiana tabacum cells is mediated by protein kinase- and anion channel-dependent release of Ca2+ from internal stores.
The source of Ca2+ involved in transducing an oxidative-burst defense signal was examined in aequorin-transformed tobacco (Nicotiana tabacum L.) cells using modulators of Ca2+ entry. Treatments that either increased or decreased the influx of Ca2+ from external stores were found to have little effect on the magnitude or kinetics of an osmotically stimulated oxidative burst. In contrast, treatments that reduced the discharge of Ca2+ from internal stores inhibited dilution-activated H2O2 production. Curiously, most of the modulators commonly employed in animal studies as internal Ca(2+)-release inhibitors were neither effective in blocking discharge of intracellular Ca2+ nor in preventing the oxidative burst. When three different biochemical elicitors of the oxidative burst were similarly examined, both the H2O2 production and Ca2+ fluxes stimulated were found to be sensitive to modulators of internal Ca2+ release, but neither was impacted by alterations in externally derived Ca2+ influx. We hypothesize, therefore, that the oxidative burst does not depend on the influx of external Ca2+, but instead may generally be mediated by the release of internal Ca2+ in a manner that depends on the proper function of kinases and anion channels. These Ca2+ pulses trigger downstream signaling events that include the activation of Ca(2+)-regulated protein kinases, which are required for stimulation of the oxidative burst.
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Biochemistry and Molecular Biology Program, Department of Chemistry, Purdue University, 1393 Brown Bldg., W. Lafayette, IN 47904, USA.
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D000331:Aequorin / Q000235:genetics / Q000502:physiology*; D001425:Bacterial Outer Membrane Proteins; D001692:Biological Transport; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000008:administration & dosage; D015220:Calcium Channels / Q000378:metabolism; D020013:Calcium Signaling / Q000502:physiology; D005658:Fungi / Q000254:growth & development; D006861:Hydrogen Peroxide / Q000378:metabolism; D007476:Ionophores / Q000008:administration & dosage; D009844:Oligosaccharides / Q000378:metabolism; D009997:Osmotic Pressure; D010100:Oxygen / Q000378:metabolism*; D030821:Plants, Genetically Modified; D011494:Protein Kinases / Q000378:metabolism*; D014026:Nicotiana / Q000187:drug effects / Q000378:metabolism* / Q000382:microbiology
D001425:Bacterial Outer Membrane Proteins; D002121:Calcium Channel Blockers; D015220:Calcium Channels; D007476:Ionophores; D009844:Oligosaccharides; C075462:harpin protein, Erwinia amylovora; C412763:oligogalacturonic acid; C087295:HrpZ protein, Pseudomonas syringae; D000331:Aequorin; D006861:Hydrogen Peroxide; D011494:Protein Kinases; D010100:Oxygen; D002118:Calcium