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Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure
Author(s) -
Huang Shouguang,
Waadt Rainer,
Nuhkat Maris,
Kollist Hannes,
Hedrich Rainer,
Roelfsema M. Rob G.
Publication year - 2019
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.15985
Subject(s) - abscisic acid , guard cell , chemistry , microbiology and biotechnology , arabidopsis , cytosol , kinase , intracellular , biophysics , protein kinase a , calcium , biology , biochemistry , enzyme , gene , organic chemistry , mutant
Summary During drought, abscisic acid (ABA) induces closure of stomata via a signaling pathway that involves the calcium (Ca 2+ )‐independent protein kinase OST1, as well as Ca 2+ ‐dependent protein kinases. However, the interconnection between OST1 and Ca 2+ signaling in ABA‐induced stomatal closure has not been fully resolved. ABA‐induced Ca 2+ signals were monitored in intact Arabidopsis leaves, which express the ratiometric Ca 2+ reporter R‐GECO1‐mTurquoise and the Ca 2+ ‐dependent activation of S‐type anion channels was recorded with intracellular double‐barreled microelectrodes. ABA triggered Ca 2+ 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 Ca 2+ signals. On average, stomata closed faster if Ca 2+ signals were elicited during the ABA response. Loss of OST1 prevented ABA‐induced stomatal closure and repressed Ca 2+ signals, whereas elevation of the cytosolic Ca 2+ concentration caused a rapid activation of SLAC1 and SLAH3 anion channels. Our data show that the majority of Ca 2+ signals are evoked during the acceleration phase of stomatal closure, which is initiated by OST1. These Ca 2+ signals are likely to activate Ca 2+ ‐dependent protein kinases, which enhance the activity of S‐type anion channels and boost stomatal closure.