Calcium signals in guard cells enhance the efficiency by which abscisic acid triggers stomatal closure
2019
Huang, Shouguang | Waadt, Rainer | Nuhkat, Maris | Kollist, Hannes | Hedrich, Rainer | Roelfsema, M. Rob G.
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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