The Guard Cell-Environment Connection

The Guard Cell-Environment Connection Department of Organismic and Evolutionary Biology, Harvard University, The Biological Laboratories, 16 Divinity Avenue, Cambridge, Massachusetts 021 38 This review surveys the signals, intermediate events, and effectors that connect GC swelling and shrinking to environmental conditions. GCs swell when protons are released, hyperpolarizing the plasma membrane (shifting the membrane potential to more negative voltages). This hyperpolarization drives K+ entry down an electrical gradient through inward K+ channels. C1- influx also occurs, presumably via Cl-/H+ symport or Cl-/OH- antiport. The entering ions are stored primarily in the vacuole along with malate, which is synthesized during stomatal opening. As intracellular osmotica increase, GCs take up water, balancing their water potential with that of their surroundings, and they begin to swell. Differential cell wall reinforcement bends the swelling GCs outward and widens the pore between them (Willmer, 1983; Taiz and Zeiger, 1991). Stomatal closure is not the reversal of opening. Anion release and/or Ca2+uptake depolarizes the plasma membrane (shifts the membrane potential to more positive values). This depolarization provides the driving force for K+ efflux through outward K+ channels. As levels of K+ and malate drop, GCs release water and shrink, relaxing the outward bend and closing over the substomatal cavity. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png

The Guard Cell-Environment Connection

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Publisher
American Society of Plant Biologist
Copyright
Copyright © 1993 by the American Society of Plant Biologists
ISSN
1532-2548
eISSN
0032-0889
Publisher site
See Article on Publisher Site

Abstract

Department of Organismic and Evolutionary Biology, Harvard University, The Biological Laboratories, 16 Divinity Avenue, Cambridge, Massachusetts 021 38 This review surveys the signals, intermediate events, and effectors that connect GC swelling and shrinking to environmental conditions. GCs swell when protons are released, hyperpolarizing the plasma membrane (shifting the membrane potential to more negative voltages). This hyperpolarization drives K+ entry down an electrical gradient through inward K+ channels. C1- influx also occurs, presumably via Cl-/H+ symport or Cl-/OH- antiport. The entering ions are stored primarily in the vacuole along with malate, which is synthesized during stomatal opening. As intracellular osmotica increase, GCs take up water, balancing their water potential with that of their surroundings, and they begin to swell. Differential cell wall reinforcement bends the swelling GCs outward and widens the pore between them (Willmer, 1983; Taiz and Zeiger, 1991). Stomatal closure is not the reversal of opening. Anion release and/or Ca2+uptake depolarizes the plasma membrane (shifts the membrane potential to more positive values). This depolarization provides the driving force for K+ efflux through outward K+ channels. As levels of K+ and malate drop, GCs release water and shrink, relaxing the outward bend and closing over the substomatal cavity.

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