title: Convergence of calcium signaling pathways of pathogenic elicitors and abscisic acid in Arabidopsis guard cells.
abstract: A variety of stimuli, such as abscisic acid (ABA), reactive oxygen species (ROS), and elicitors of plant defense reactions, have been shown to induce stomatal closure. Our study addresses commonalities in the signaling pathways that these stimuli trigger. A recent report showed that both ABA and ROS stimulate an NADPH-dependent, hyperpolarization-activated Ca(2+) influx current in Arabidopsis guard cells termed "I(Ca)" (Z.M. Pei, Y. Murata, G. Benning, S. Thomine, B. Klüsener, G.J. Allen, E. Grill, J.I. Schroeder, Nature [2002] 406: 731-734). We found that yeast (Saccharomyces cerevisiae) elicitor and chitosan, both elicitors of plant defense responses, also activate this current and activation requires cytosolic NAD(P)H. These elicitors also induced elevations in the concentration of free cytosolic calcium ([Ca(2+)](cyt)) and stomatal closure in guard cells. ABA and ROS elicited [Ca(2+)](cyt) oscillations in guard cells only when extracellular Ca(2+) was present. In a 5 mM KCl extracellular buffer, 45% of guard cells exhibited spontaneous [Ca(2+)](cyt) oscillations that differed in their kinetic properties from ABA-induced Ca(2+) increases. These spontaneous [Ca(2+)](cyt) oscillations also required the availability of extracellular Ca(2+) and depended on the extracellular potassium concentration. Interestingly, when ABA was applied to spontaneously oscillating cells, ABA caused cessation of [Ca(2+)](cyt) elevations in 62 of 101 cells, revealing a new mode of ABA signaling. These data show that fungal elicitors activate a shared branch with ABA in the stress signal transduction pathway in guard cells that activates plasma membrane I(Ca) channels and support a requirement for extracellular Ca(2+) for elicitor and ABA signaling, as well as for cellular [Ca(2+)](cyt) oscillation maintenance.
authors.affiliation: Cell and Developmental Biology Section, Division of Biology, and Center for Molecular Genetics, University of California, San Diego, La Jolla, California 92093-0116, USA.
authors.forename: Birgit
authors.initials: B
authors.lastname: Klüsener
authors.forename: Jared J
authors.initials: JJ
authors.lastname: Young
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Murata
authors.forename: Gethyn J
authors.initials: GJ
authors.lastname: Allen
authors.forename: Izumi C
authors.initials: IC
authors.lastname: Mori
authors.forename: Veronique
authors.initials: V
authors.lastname: Hugouvieux
authors.forename: Julian I
authors.initials: JI
authors.lastname: Schroeder
mesh_terms: D000040:Abscisic Acid / Q000494:pharmacology*; D017360:Arabidopsis / Q000187:drug effects* / Q000382:microbiology / Q000502:physiology; D002118:Calcium / Q000378:metabolism / Q000494:pharmacology; D002120:Calcium Channel Agonists / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology*; D002686:Chitin / Q000031:analogs & derivatives* / Q000494:pharmacology; D048271:Chitosan; D003600:Cytosol / Q000378:metabolism; D005658:Fungi / Q000254:growth & development; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007113:Immunity, Innate / Q000502:physiology; D008564:Membrane Potentials / Q000187:drug effects; D009249:NADP / Q000494:pharmacology; D009536:Niacinamide / Q000494:pharmacology; D019441:Plant Epidermis / Q000166:cytology / Q000187:drug effects* / Q000382:microbiology; D017382:Reactive Oxygen Species / Q000494:pharmacology; D012441:Saccharomyces cerevisiae / Q000254:growth & development; D015398:Signal Transduction / Q000187:drug effects
chemical_list: D002120:Calcium Channel Agonists; D015220:Calcium Channels; D017382:Reactive Oxygen Species; D002686:Chitin; D009536:Niacinamide; D009249:NADP; D000040:Abscisic Acid; D048271:Chitosan; D006861:Hydrogen Peroxide; D002118:Calcium