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Involvement of intracellular Ca 2+ in blue light‐dependent proton pumping in guard cell protoplasts from Vicia faba
Author(s) -
Shimazaki K.,
Goh C.H.,
Kinoshita T.
Publication year - 1999
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1034/j.1399-3054.1999.105322.x
Subject(s) - guard cell , cyclopiazonic acid , thapsigargin , intracellular , biophysics , chemistry , endoplasmic reticulum , vicia faba , calmodulin , caffeine , biochemistry , atpase , biology , botany , enzyme , endocrinology
Recent studies have suggested that Ca 2+ /calmodulin (CaM) or CaM‐like proteins may be involved in blue light (BL)‐dependent proton pumping in guard cells. As the increase in cytosolic concentration of Ca 2+ is required for the activation of CaM and CaM‐like proteins, the origin of the Ca 2+ was investigated by measuring BL‐dependent proton pumping with various treatments using guard cell protoplasts (GCPs) from Vicia faba . BL‐dependent proton pumping was affected neither by Ca 2+ channel blockers nor by changes of Ca 2+ concentration in the medium used for the GCPs. Addition of Ca 2+ ionophores and an agonist to GCPs did not induce proton pumping. However, BL‐dependent proton pumping was inhibited by 10 m M caffeine, which releases Ca 2+ from the intracellular stores, and by 10 μ M 2,5‐di‐( tert ‐butyl)‐1,4‐benzohydroquinone (BHQ) and 10 μ M cyclopiazonic acid (CPA), inhibitors of Ca 2+ ‐ATPase in the sarcoplasmic and endoplasmic reticulum (ER). By contrast, the inhibitions were not observed by 10 μ M thapsigargin, an inhibitor of animal ER‐type Ca 2+ ‐ATPase. The inhibitions by caffeine and BHQ were reversible. Light‐dependent stomatal opening in the epidermis of Vicia was inhibited by caffeine, BHQ, and CPA. From these results, we conclude that the Ca 2+ thought to be required for BL‐dependent proton pumping may originate from intracellular Ca 2+ stores, most likely from ER in guard cells, and that this origin of Ca 2+ may generate a stimulus‐specific Ca 2+ signal for stomatal opening.