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Calcium elevation‐dependent and attenuated resting calcium‐dependent abscisic acid induction of stomatal closure and abscisic acid‐induced enhancement of calcium sensitivities of S‐type anion and inward‐rectifying K + channels in Arabidopsis guard cells
Author(s) -
Siegel Robert S.,
Xue Shaowu,
Murata Yoshiyuki,
Yang Yingzhen,
Nishimura Noriyuki,
Wang Angela,
Schroeder Julian I.
Publication year - 2009
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2009.03872.x
Subject(s) - abscisic acid , guard cell , biology , biophysics , calcium , resting potential , biochemistry , microbiology and biotechnology , chemistry , membrane potential , organic chemistry , gene
Summary Stomatal closure in response to abscisic acid depends on mechanisms that are mediated by intracellular [Ca 2+ ] ([Ca 2+ ] i ), and also on mechanisms that are independent of [Ca 2+ ] i in guard cells. In this study, we addressed three important questions with respect to these two predicted pathways in Arabidopsis thaliana . (i) How large is the relative abscisic acid (ABA)‐induced stomatal closure response in the [Ca 2+ ] i ‐elevation‐independent pathway? (ii) How do ABA‐insensitive mutants affect the [Ca 2+ ] i ‐elevation‐independent pathway? (iii) Does ABA enhance (prime) the Ca 2+ sensitivity of anion and inward‐rectifying K + channel regulation? We monitored stomatal responses to ABA while experimentally inhibiting [Ca 2+ ] i elevations and clamping [Ca 2+ ] i to resting levels. The absence of [Ca 2+ ] i elevations was confirmed by ratiometric [Ca 2+ ] i imaging experiments. ABA‐induced stomatal closure in the absence of [Ca 2+ ] i elevations above the physiological resting [Ca 2+ ] i showed only approximately 30% of the normal stomatal closure response, and was greatly slowed compared to the response in the presence of [Ca 2+ ] i elevations. The ABA‐insensitive mutants ost1‐2 , abi2‐1 and gca2 showed partial stomatal closure responses that correlate with [Ca 2+ ] i ‐dependent ABA signaling. Interestingly, patch‐clamp experiments showed that exposure of guard cells to ABA greatly enhances the ability of cytosolic Ca 2+ to activate S‐type anion channels and down‐regulate inward‐rectifying K + channels, providing strong evidence for a Ca 2+ sensitivity priming hypothesis. The present study demonstrates and quantifies an attenuated and slowed ABA response when [Ca 2+ ] i elevations are directly inhibited in guard cells. A minimal model is discussed, in which ABA enhances (primes) the [Ca 2+ ] i sensitivity of stomatal closure mechanisms.