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

Stephen G. Cessna, Philip Low

Research output: Contribution to journalArticle

39 Scopus citations

Abstract

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 Ca2+-release inhibitors were neither effective in blocking discharge of intracellular C2+ 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+ reflux. 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 Ca2+-regulated protein kinases, which are required for stimulation of the oxidative burst.

Original languageEnglish (US)
Pages (from-to)126-134
Number of pages9
JournalPlanta
Volume214
Issue number1
DOIs
StatePublished - Jan 1 2001

Keywords

  • Calcium
  • Nicotiana (oxidative burst)
  • Oxidative burst
  • Signal transduction

ASJC Scopus subject areas

  • Plant Science

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