Journal
NEW PHYTOLOGIST
Volume 224, Issue 1, Pages 177-187Publisher
WILEY
DOI: 10.1111/nph.15985
Keywords
abscisic acid (ABA); Ca2+-indicator; cytosolic Ca2+ signals; OST1 protein kinase; R-GECO1-mTurquoise; SLAC1 and SLAH3 anion channels; stomata
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Funding
- Germany Science Foundation (DFG) 'Pathogate': Stomatal control of pathogenic microbe infestation [HE 1640/34-1, RO 2381/6-1]
- DFG [WA 3768/1-1]
- China Scholarship Council (CSC) [201506350031]
- Estonian Research Council [IUT2-21]
- European Regional Development Fund (Centre of Excellence in Molecular Cell Engineering)
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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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