1997
DOI: 10.1093/oxfordjournals.pcp.a029230
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Inhibition of the Stomatal Blue Light Response by Verapamil at High Concentration

Abstract: Blue light-dependent proton pumping in guard cell protoplasts and light-induced stomatal opening in the epidermis were inhibited by 1 mM verapamil, a Ca2+ channel blocker. Proton pumping and stomatal opening induced by fusicoccin, an activator of plasma membrane proton pump, were not inhibited by verapamil. These results suggest that verapamil inhibits blue light signaling in guard cells without inhibiting the pump.

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Cited by 19 publications
(10 citation statements)
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“…The kinetics of the blue light-dependent acidification of the external medium closely matched that observed for stomatal opening in intact leaves. It was postulated that blue light activates the plasma membrane H + -ATPase via Ca 2 + -dependent pathways, probably also including protein phosphorylation [108][109][110]. The H + extrusion observed by Shimazaki et al [107] was in accordance with electrophysiological studies demonstrating membrane hyperpolarization in response to blue light [97].…”
Section: Blue Light and Membrane Hyperpolarizationmentioning
confidence: 62%
“…The kinetics of the blue light-dependent acidification of the external medium closely matched that observed for stomatal opening in intact leaves. It was postulated that blue light activates the plasma membrane H + -ATPase via Ca 2 + -dependent pathways, probably also including protein phosphorylation [108][109][110]. The H + extrusion observed by Shimazaki et al [107] was in accordance with electrophysiological studies demonstrating membrane hyperpolarization in response to blue light [97].…”
Section: Blue Light and Membrane Hyperpolarizationmentioning
confidence: 62%
“…Calmodulin antagonists inhibited both blue-light-dependent H + pumping and stomatal opening (158). The pumping was inhibited by verapamil, a Ca 2+ channel blocker, albeit at high concentrations (160). The H + pumping was inhibited reversibly by caffeine, which releases Ca 2+ from intracellular stores, and by inhibitors of endoplasmic reticulum Ca 2+ -ATPase.…”
Section: Vfpip a Protein Interacting Withmentioning
confidence: 99%
“…Here we report genetic, biochemical and signaling network mechanisms that underpin this cellular response. In the absence of ABA, Ca 2+ responsiveness is inhibited by PP2Cs, thereby preventing responses to unrelated stomatal opening-mediating stimuli (Irving et al, 1992;Shimazaki et al, 1992;Curvetto et al, 1994;Shimazaki et al, 1997;Cousson and Vavasseur, 1998;Young et al, 2006) and also spontaneous Ca 2+ elevations (Young et al, 2006;Siegel et al, 2009). As PP2Cs inhibit OST1 and also down-regulate SLAC1 directly, this network not only enables stimulus specific activation of SLAC1, but also provides a tight off switch via PP2C-catalyzed dephosphorylation of (Figure 7).…”
Section: Discussionmentioning
confidence: 99%
“…Simplified schematic model for Ca 2+ -specificity mechanism within ABA-dependent SLAC1 activation in guard cells. (A) Without ABA, Ca 2+ elevations that can also function in stomatal opening responses (Irving et al, 1992;Shimazaki et al, 1992;Curvetto et al, 1994;Shimazaki et al, 1997;Cousson and Vavasseur, 1998;Young et al, 2006) and spontaneous or un-specifically induced Ca 2+ transients (Allen et al, 1999b;Klüsener et al, 2002;Young et al, 2006;Yang et al, 2008;Siegel et al, 2009) do not lead to S-type anion channel (SLAC1) activation as PP2C protein phosphatases directly negatively regulate SLAC1 activation. (B) In the presence of ABA this SLAC1 inhibition is released, OST1 and CPKs phosphorylate, and thereby activate the channel.…”
Section: Discussionmentioning
confidence: 99%