• Medientyp: E-Artikel
  • Titel: Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure
  • Beteiligte: Huang, Shouguang; Waadt, Rainer; Nuhkat, Maris; Kollist, Hannes; Hedrich, Rainer; Roelfsema, M. Rob G.
  • Erschienen: Wiley, 2019
  • Erschienen in: New Phytologist, 224 (2019) 1, Seite 177-187
  • Sprache: Englisch
  • DOI: 10.1111/nph.15985
  • ISSN: 0028-646X; 1469-8137
  • Entstehung:
  • Anmerkungen:
  • Beschreibung: SummaryDuring drought, abscisic acid (ABA) induces closure of stomata via a signaling pathway that involves the calcium (Ca2+)‐independent protein kinase OST1, as well as Ca2+‐dependent protein kinases. However, the interconnection between OST1 and Ca2+ signaling in ABA‐induced stomatal closure has not been fully resolved.ABA‐induced Ca2+ signals were monitored in intact Arabidopsis leaves, which express the ratiometric Ca2+ reporter R‐GECO1‐mTurquoise and the Ca2+‐dependent activation of S‐type anion channels was recorded with intracellular double‐barreled microelectrodes.ABA triggered Ca2+ signals that occurred during the initiation period, as well as in the acceleration phase of stomatal closure. However, a subset of stomata closed in the absence of Ca2+ signals. On average, stomata closed faster if Ca2+ signals were elicited during the ABA response. Loss of OST1 prevented ABA‐induced stomatal closure and repressed Ca2+ signals, whereas elevation of the cytosolic Ca2+ concentration caused a rapid activation of SLAC1 and SLAH3 anion channels.Our data show that the majority of Ca2+ signals are evoked during the acceleration phase of stomatal closure, which is initiated by OST1. These Ca2+ signals are likely to activate Ca2+‐dependent protein kinases, which enhance the activity of S‐type anion channels and boost stomatal closure.
  • Zugangsstatus: Freier Zugang