ArticleThe Journal of membrane biology1992
Permeation of Ca2+ through K+ channels in the plasma membrane of Vicia faba guard cells.
Article in The Journal of membrane biology, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 77 citations in OpenAlex.
- Molecular Evolution and Interaction of Membrane Transport and Photoreception in Plants.Frontiers in genetics · 2019Review
- Interaction between Calcium and Actin in Guard Cell and Pollen Signaling Networks.Plants (Basel, Switzerland) · 2013Review
- Regulation by external K+ in a maize inward shaker channel targets transport activity in the high concentration range.The Plant cell · 2005Article
- AKT2/3 subunits render guard cell K+ channels Ca2+ sensitive.The Journal of general physiology · 2005Article
- Opposing effects of aluminum on inward-rectifier potassium currents in bean root-tip protoplasts.The Journal of membrane biology · 2004Article
- Sodium fluxes through nonselective cation channels in the plasma membrane of protoplasts from Arabidopsis roots.Plant physiology · 2002Article
- Extracellular protons inhibit the activity of inward-rectifying potassium channels in the motor cells of Samanea saman pulvini.Plant physiology · 2001Article
- KAT1 is not essential for stomatal opening.Proceedings of the National Academy of Sciences of the United States of America · 2001Article
- Hyperpolarization-activated calcium channels at the tip of Arabidopsis root hairs.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Inositol hexakisphosphate is a physiological signal regulating the K+-inward rectifying conductance in guard cells.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- Ca2+ channels at the plasma membrane of stomatal guard cells are activated by hyperpolarization and abscisic acid.Proceedings of the National Academy of Sciences of the United States of America · 2000Article
- AKT3, a phloem-localized K+ channel, is blocked by protons.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
- A steep dependence of inward-rectifying potassium channels on cytosolic free calcium concentration increase evoked by hyperpolarization in guard cellsPlant physiology · 1999Article
- Spatial Organization of Calcium Signaling Involved in Cell Volume Control in the Fucus Rhizoid.The Plant cell · 1996Article
- Membrane-Delimited Phosphorylation Enables the Activation of the Outward-Rectifying K Channels in Motor Cell Protoplasts of Samanea saman.Plant physiology · 1996Article
- Changes in voltage activation, Cs+ sensitivity, and ion permeability in H5 mutants of the plant K+ channel KAT1.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- The Role of Potassium Channels in the Temperature Control of Stomatal Aperture.Plant physiology · 1995Article
- Is ATP Required for K+ Channel Activation in Vicia Guard Cells?Plant physiology · 1995Article
- Properties of the K+ inward rectifier in the plasma membrane of xylem parenchyma cells from barley roots: effects of TEA+, Ca2+, Ba2+ and La3+.The Journal of membrane biology · 1994Article
- Green circuits--the potential of plant specific ion channels.Plant molecular biology · 1994Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The whole-cell patch-clamp method has been used to measure Ca2+ influx through otherwise K(+)-selective channels in the plasma membrane surrounding protoplasts from guard cells of Vicia faba. These channels are activated by membrane hyperpolarization. The resulting K+ influx contributes to the increase in guard cell turgor which causes stomatal opening during the regulation of leaf-air gas exchange. We find that after opening the K+ channels by hyperpolarization, depolarization of the membrane results in tail current at voltages where there is no electrochemical force to drive K+ inward through the channels. Tail current remains when the reversal potential for permeant ions other than Ca2+ is more negative than or equal to the K+ equilibrium potential (-47 mV), indicating that the current is due to Ca2+ influx through the K+ channels prior to their closure. Decreasing internal [Ca2+] (Cai) from 200 to 2 nM or increasing the external [Ca2+] (Cao) from 1 to 10 mM increases the amplitude of tail current and shifts the observed reversal potential to more positive values. Such increases in the electrochemical force driving Ca2+ influx also decrease the amplitude of time-activated current, indicating that Ca2+ permeation is slower than K+ permeation, and so causes a partial block. Increasing Cao also (i) causes a positive shift in the voltage dependence of current, presumably by decreasing the membrane surface potential, and (ii) results in a U-shaped current-voltage relationship with peak inward current ca. -160 mV, indicating that the Ca2+ block is voltage dependent and suggesting that the cation binding site is within the electric field of the membrane. K+ channels in Zea mays guard cells also appear to have a Cai- and Cao-dependent ability to mediate Ca2+ influx. We suggest that the inwardly rectifying K+ channels are part of a regulatory mechanism for Cai. Changes in Cao and (associated) changes in Cai regulate a variety of intracellular processes and ion fluxes, including the K+ and anion fluxes associated with stomatal aperture change.
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