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PMID:19302418

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Citation

Siegel, RS, Xue, S, Murata, Y, Yang, Y, Nishimura, N, Wang, A and Schroeder, JI (2009) 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. Plant J. 59:207-20

Abstract

Stomatal closure in response to abscisic acid depends on mechanisms that are mediated by intracellular [Ca2+] ([Ca2+]i), and also on mechanisms that are independent of [Ca2+]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 [Ca2+]i-elevation-independent pathway? (ii) How do ABA-insensitive mutants affect the [Ca2+]i-elevation-independent pathway? (iii) Does ABA enhance (prime) the Ca2+ sensitivity of anion and inward-rectifying K+ channel regulation? We monitored stomatal responses to ABA while experimentally inhibiting [Ca2+]i elevations and clamping [Ca2+]i to resting levels. The absence of [Ca2+]i elevations was confirmed by ratiometric [Ca2+]i imaging experiments. ABA-induced stomatal closure in the absence of [Ca2+]i elevations above the physiological resting [Ca2+]i showed only approximately 30% of the normal stomatal closure response, and was greatly slowed compared to the response in the presence of [Ca2+]i elevations. The ABA-insensitive mutants ost1-2, abi2-1 and gca2 showed partial stomatal closure responses that correlate with [Ca2+]i-dependent ABA signaling. Interestingly, patch-clamp experiments showed that exposure of guard cells to ABA greatly enhances the ability of cytosolic Ca2+ to activate S-type anion channels and down-regulate inward-rectifying K+ channels, providing strong evidence for a Ca2+ sensitivity priming hypothesis. The present study demonstrates and quantifies an attenuated and slowed ABA response when [Ca2+]i elevations are directly inhibited in guard cells. A minimal model is discussed, in which ABA enhances (primes) the [Ca2+]i sensitivity of stomatal closure mechanisms.

Links

PubMed PMC2827207 Online version:10.1111/j.1365-313X.2009.03872.x

Keywords

Abscisic Acid/pharmacology; Arabidopsis/genetics; Arabidopsis/metabolism; Arabidopsis/physiology; Arabidopsis Proteins/genetics; Arabidopsis Proteins/metabolism; Calcium/metabolism; Ion Channel Gating; Mutation; Patch-Clamp Techniques; Plant Stomata/metabolism; Plant Stomata/physiology; Potassium Channels, Inwardly Rectifying/genetics; Potassium Channels, Inwardly Rectifying/metabolism

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status

ARATH:F4JGW8

acts_upstream_of_or_within

GO:0010119: regulation of stomatal movement

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete

ARATH:F4JGW8

acts_upstream_of_or_within

GO:0009737: response to abscisic acid

ECO:0000315: mutant phenotype evidence used in manual assertion

P

Seeded From UniProt

complete


See also

References

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