title: Protein phosphorylation is a prerequisite for intracellular Ca2+ release and ion channel control by nitric oxide and abscisic acid in guard cells.
abstract: Recent work has indicated that nitric oxide (NO) and its synthesis are important elements of signal cascades in plant-pathogen defence, and are a prerequisite for drought and abscisic acid (ABA) responses in Arabidopsis thaliana and Vicia faba guard cells. NO regulates inward-rectifying K+ channels and Cl- channels of Vicia guard cells via intracellular Ca2+ release. However, its integration with related signals, including the actions of serine-threonine protein kinases, is less well defined. We report here that the elevation of cytosolic-free [Ca2+] ([Ca2+]i) mediated by NO in guard cells is reversibly inhibited by the broad-range protein kinase antagonists staurosporine and K252A, but not by the tyrosine kinase antagonist genistein. The effects of kinase antagonism translate directly to a loss of NO-sensitivity of the inward-rectifying K+ channels and background (Cl- channel) current, and to a parallel loss in sensitivity of the K+ channels to ABA. These results demonstrate that NO-dependent signals can be modulated through protein phosphorylation upstream of intracellular Ca2+ release, and they implicate a target for protein kinase control in ABA signalling that feeds into NO-dependent Ca2+ release.
authors.affiliation: Laboratory of Plant Physiology and Biophysics, Bower Building, Institute of Biomedical and Life Sciences, University of Glasgow, Glasgow G12 8QQ, UK.
authors.forename: Sergei
authors.initials: S
authors.lastname: Sokolovski
authors.forename: Adrian
authors.initials: A
authors.lastname: Hills
authors.forename: Rob
authors.initials: R
authors.lastname: Gay
authors.forename: Carlos
authors.initials: C
authors.lastname: Garcia-Mata
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Lamattina
authors.forename: Michael R
authors.initials: MR
authors.lastname: Blatt
mesh_terms: D000040:Abscisic Acid / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D020013:Calcium Signaling / Q000502:physiology; D002227:Carbazoles / Q000494:pharmacology; D002462:Cell Membrane / Q000502:physiology; D019833:Genistein / Q000494:pharmacology; D026121:Indole Alkaloids; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D009569:Nitric Oxide / Q000502:physiology*; D010766:Phosphorylation; D010940:Plant Proteins / Q000378:metabolism*; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D011494:Protein Kinases / Q000378:metabolism; D011499:Protein Processing, Post-Translational; D019311:Staurosporine / Q000494:pharmacology; D031307:Vicia faba / Q000166:cytology / Q000502:physiology*
chemical_list: D002227:Carbazoles; D026121:Indole Alkaloids; D007473:Ion Channels; D010940:Plant Proteins; D047428:Protein Kinase Inhibitors; D009569:Nitric Oxide; D000040:Abscisic Acid; C049985:staurosporine aglycone; D019833:Genistein; D011494:Protein Kinases; D019311:Staurosporine; D002118:Calcium