Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure

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 bee...

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Hauptverfasser: Huang, Shouguang (VerfasserIn) , Waadt, Rainer (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 10 June 2019
In: The new phytologist
Year: 2019, Jahrgang: 224, Heft: 1, Pages: 177-187
ISSN:1469-8137
DOI:10.1111/nph.15985
Online-Zugang:Verlag, Volltext: https://doi.org/10.1111/nph.15985
Verlag: https://nph.onlinelibrary.wiley.com/doi/abs/10.1111/nph.15985
Volltext
Verfasserangaben:Shouguang Huang, Rainer Waadt, Maris Nuhkat, Hannes Kollist, Rainer Hedrich and M. Rob G. Roelfsema

MARC

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520 |a 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. 
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