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.
by Siegel R. S., Xue S., Murata Y., Yang Y., Nishimura N., Wang A., Schroeder J. I. (2009)
in Plant J. 59, 207–220. – doi: 10.1111/j.1365-313X.2009.03872.x –
Stomatal closure in response to abscisic acid depends on mechanisms that are mediated by intracellular [Ca2+] ([Ca2+]i), and also on mechanisms independent of [Ca2+]i in guard cells.
In this study we address three important questions in reference to these two predicted pathways in Arabidopsis thaliana.
1. How large is the relative abscisic acid (ABA)-induced stomatal closing response from a [Ca2+]i-elevation-independent pathway?
2. How do ABA-insensitive mutants affect a [Ca2+]i-elevation-independent pathway?
3. 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 in ratiometric [Ca2+]i imaging experiments.
ABA-induced stomatal closing in the absence of [Ca2+]i-elevations above the physiological resting [Ca2+]i showed only ≈30% of the stomatal closure response and was greatly slowed compared to the presence of [Ca2+]i-elevations.
The ABA-insensitive mutants ost1-2, abi2-1, gca2 showed partial stomatal closing responses that correlate with [Ca2+]i-dependent ABA signaling. Interestingly, patch clamp experiments show that exposure of guard cells to ABA greatly enhances the ability of cytosolic Ca2+to both activate S-type anion channels and down-regulate inward K+ channels, providing strong evidence for the Ca2+ sensitivity priming hypothesis.
The present study shows and quantifies an attenuated and slowed ABA response, while directly inhibiting [Ca2+]i-elevations in guard cells. A minimal model is discussed, in which ABA increases (primes) the [Ca2+]i sensitivity of stomatal closing mechanisms.