* During 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.
%0 Journal Article
%1 noauthororeditorcalcium
%A Huang, Shouguang
%A Waadt, Rainer
%A Nuhkat, Maris
%A Kollist, Hannes
%A Hedrich, Rainer
%A Roelfsema, M. Rob G.
%D 2019
%J New Phytologist
%K , Abscisic Acid, R-GECO1-mTurquoise SLAC1, SLAH3,ABA, anion ca2+-signals, channel, ejection, guard-cell, myown nano
%R doi: 10.1111/nph.15985
%T Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure
%X * During 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.
@article{noauthororeditorcalcium,
abstract = {* During 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.},
added-at = {2019-07-25T10:44:44.000+0200},
author = {Huang, Shouguang and Waadt, Rainer and Nuhkat, Maris and Kollist, Hannes and Hedrich, Rainer and Roelfsema, M. Rob G.},
biburl = {https://www.bibsonomy.org/bibtex/200cd6fa88ca7df25a749082107ca957a/robroelfsema},
doi = {doi: 10.1111/nph.15985},
interhash = {56b2096c7c01f9c0ec5376f884d2ca02},
intrahash = {00cd6fa88ca7df25a749082107ca957a},
journal = {New Phytologist},
keywords = {, Abscisic Acid, R-GECO1-mTurquoise SLAC1, SLAH3,ABA, anion ca2+-signals, channel, ejection, guard-cell, myown nano},
timestamp = {2019-07-25T10:44:44.000+0200},
title = {Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure},
year = 2019
}