Calcium-Activated K + Channels and Calcium-Induced Calcium Release by Slow Vacuolar Ion Channels in Guard Cell Vacuoles Implicated in the Control of Stomatal Closure

1994 ◽  
Vol 6 (5) ◽  
pp. 669 ◽  
Author(s):  
John M. Ward ◽  
Julian I. Schroeder
Keyword(s):  
Ion Channels ◽  
Guard Cell ◽  
Calcium Release ◽  
Stomatal Closure ◽  
K Channels ◽  
Calcium Induced Calcium Release

scholarly journals Signal transduction and ion channels in guard cells

1998 ◽  
Vol 353 (1374) ◽  
pp. 1475-1488 ◽  
Author(s):  
E. A. C. MacRobbie
Keyword(s):  
Membrane Potential ◽  
Ion Channels ◽  
Phospholipase C ◽  
Guard Cell ◽  
Protein Phosphatase ◽  
Stomatal Closure ◽  
Anion Channel ◽  
Cytoplasmic Ph ◽  
Anion Channels ◽  
Sv Channel

Our understanding of the signalling mechanisms involved in the process of stomatal closure is reviewed. Work has concentrated on the mechanisms by which abscisic acid (ABA) induces changes in specific ion channels at both the plasmalemma and the tonoplast leading to efflux of both K + and anions at both membranes, requiring four essential changes. For each we need to identify the specific channels concerned, and the detailed signalling chains by which each is linked through signalling intermediates to ABA. There are two global changes that are identified following ABA treatment, an increase in cytoplasmic pH and an increase in cytoplasmic Ca 2+ , although stomata can close without any measurable global increase in cytoplasmic Ca 2+ . There is also evidence for the importance of several protein phosphatases and protein kinases in the regulation of channel activity. At the plasmalemma, loss of K + requires depolarization of the membrane potential into the range at which the outward K + channel is open. ABA–induced activation of a non–specific cation channel, permeable to Ca 2+ , may contribute to the necessary depolarization, together with ABA–induced activation of S–type anion channels in the plasmalemma, which are then responsible for the necessary anion efflux. The anion channels are activated by Ca 2+ and by phosphorylation, but the precise mechanism of their activation by ABA is not yet clear. ABA also up–regulates the outward K + current at any given membrane potential; this activation is Ca 2+ –independent and is attributed to the increase in cytoplasmic pH, perhaps through the marked pH–sensitivity of protein phosphatase type 2C. Our understanding of mechanisms at the tonoplast is much less complete. A total of two channels, both Ca 2+ –activated, have been identified which are capable of K + efflux; these are the voltage–independent VK channel specific to K + , and the slow vacuolar (SV) channel which opens only at non–physiological tonoplast potentials (cytoplasm positive). The SV channel is permeable to K + and Ca 2+ , and although it has been argued that it could be responsible for Ca 2+ –induced Ca 2+ release, it now seems likely that it opens only under conditions where Ca 2+ will flow from cytoplasm to vacuole. Although tracer measurements show unequivocally that ABA does activate efflux of Cl – from vacuole to cytoplasm, no vacuolar anion channel has yet been identified. There is clear evidence that ABA activates release of Ca 2+ from internal stores, but the source and trigger for ABA–induced increase in cytoplasmic Ca 2+ are uncertain. The tonoplast and another membrane, probably ER, have IP 3 –sensitive Ca 2+ release channels, and the tonoplast has also cADPR–activated Ca 2+ channels. Their relative contributions to ABA–induced release of Ca 2+ from internal stores remain to be established. There is some evidence for activation of phospholipase C by ABA, by an unknown mechanism; plant phospholipase C may be activated by Ca 2+ rather than by the G–proteins used in many animal cell signalling systems. A further ABA–induced channel modulation is the inhibition of the inward K + channel, which is not essential for closing but will prevent opening. It is suggested that this is mediated through the Ca 2+ –activated protein phosphatase, calcineurin. The question of Ca 2+ –independent stomatal closure remains controversial. At the plasmalemma the stimulation of K + efflux is Ca 2+ –independent and, at least in Arabidopsis , activation of anion efflux by ABA may also be Ca 2+ –independent. But there are no indications of Ca 2+ –independent mechanisms for K + efflux at the tonoplast, and the appropriate anion channel at the tonoplast is still to be found. There is also evidence that ABA interferes with a control system in the guard cell, resetting its set–point to lower contents, suggesting that stretch–activated channels also feature in the regulation of guard cell ion channels, perhaps through interactions with cytoskeletal proteins. There is evidence for involvement of actin in the control of guard cell ion channels, although possible mechanisms are still to be identified. Stomatal closure involves net loss of vacuolar sugars as well as potassium salts, and there is an urgent need to address the question of the nature of the signalling chains linking transport and metabolism of sugars to the closing signal.

scholarly journals Structural and Functional Insights into the Role of Guard Cell Ion Channels in Abiotic Stress-Induced Stomatal Closure

Plants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 2774
Author(s):  
Hamdy Kashtoh ◽  
Kwang-Hyun Baek
Keyword(s):  
Ion Channels ◽  
Guard Cell ◽  
Stomatal Closure ◽  
Turgor Pressure ◽  
Anion Channel ◽  
Weather Conditions ◽  
Guard Cells ◽  
Water Transpiration ◽  
Structure And Functions

A stomatal pore is formed by a pair of specialized guard cells and serves as a major gateway for water transpiration and atmospheric CO2 influx for photosynthesis in plants. These pores must be tightly controlled, as inadequate CO2 intake and excessive water loss are devastating for plants. When the plants are exposed to extreme weather conditions such as high CO2 levels, O3, low air humidity, and drought, the turgor pressure of the guard cells exhibits an appropriate response against these stresses, which leads to stomatal closure. This phenomenon involves a complex network of ion channels and their regulation. It is well-established that the turgor pressure of guard cells is regulated by ions transportation across the membrane, such as anions and potassium ions. In this review, the guard cell ion channels are discussed, highlighting the structure and functions of key ion channels; the SLAC1 anion channel and KAT1 potassium channel, and their regulatory components, emphasizing their significance in guard cell response to various stimuli.

Calcium imaging of mechanically induced fluxes in tissue-cultured chick heart: role of stretch-activated ion channels

1992 ◽  
Vol 262 (4) ◽  
pp. H1110-H1115 ◽  
Author(s):  
W. Sigurdson ◽  
A. Ruknudin ◽  
F. Sachs
Keyword(s):  
Ion Channels ◽  
Calcium Release ◽  
Heart Cells ◽  
Mechanical Stimuli ◽  
Extracellular Medium ◽  
Fluorescent Response ◽  
Chick Heart ◽  
Calcium Induced Calcium Release ◽  
Stretch Activated Ion Channels

Heart rate and contractility are sensitive to stretch. To better understand the origin of these effects, we have studied the effect of mechanical stimuli on a model system of tissue-cultured heart cells. Gently prodding cells with a pipette produced a Ca2+ influx that often led to waves of calcium-induced calcium release (CICR) spreading from the site of stimulation. Ca2+ release could also be produced by pulling on neighboring cells. The response was blocked by removing extracellular Ca2+ or by adding 20 microM Gd3+ to normal saline. The mechanical sensitivity probably arose from stretch-activated ion channels (SACs) based on several lines of evidence. Chick heart cells contain nonselective cation SACs that pass Ca2+ as well as Na+ and K+. Both the SACs and the fluorescence response are blocked by 20 microM Gd3+. Removal of Ca2+ from the extracellular medium blocked the fluorescent response. Cultures without SACs (grown in the absence of embryo extract) had no mechanically induced fluxes. These data contradict the recent claim that SAC activity is a patch-clamp artifact (C.E. Morris and R. Horn, Science Wash. DC 256: 1246-1249, 1991). The SACs had a density of approximately 1/micron 2 and were expected to pass less than 20 fA of Ca2+ current under physiological conditions. The change in intracellular concentration of Ca2+ ([Ca2+]i) resulting from activation of SACs may be too small to induce CICR unless the channels pass current into a restricted space (N. LeBlanc and J.R. Hume, Science Wash. DC 248: 372, 1990).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Ozone Altered Stomatal/Guard Cell Function: Whole Plant and Single Cell Analysis

2000 ◽  
Author(s):  
Eva J. Pell ◽  
Sarah M. Assmann ◽  
Amnon Schwartz ◽  
Hava Steinberger
Keyword(s):  
Hydrogen Peroxide ◽  
Gas Exchange ◽  
Vicia Faba ◽  
Guard Cell ◽  
Cell Function ◽  
Stomatal Closure ◽  
Relative Sensitivity ◽  
Guard Cells ◽  
Stomatal Opening ◽  
K Channels

Original objectives (revisions from original proposal are highlighted) 1. Elucidate the direct effects O3 and H2O2 on guard cell function, utilizing assays of stomatal response in isolated epidermal peels and whole cell gas exchange. 2. Determine the mechanistic basis of O3 and H2O2 effects on the plasma membrane through application of the electrophysiological technique of patch clamping to isolated guard cells. 3. Determine the relative sensitivity of Israeli cultivars of economically important crops to O3 and determine whether differential leaf conductance responses to O3 can explain relative sensitivity to the air pollutant: transfer of technological expertise to Israel. Background to the topic For a long time O3 has been known to reduce gas exchange in plants; it has however been unclear if O3 can affect the stomatal complex directly. Ion channels are essential in stomatal regulation, but O3 has never before been shown to affect these directly. Major conclusions, solution, achievements 1. Ozone inhibits light-induced stomatal opening in epidermal peels isolated from Vicia faba, Arabidopsis thaliana and Nicotiana tabacum in V. faba plants this leads to reduced assimilation without a direct effect on the photosynthetic apparatus. Stomatal opening is more sensitive to O3 than stomatal closure. 2. Ozone causes inhibition of inward K+ channels (involved in stomatal opening) while no detectable effect is observed o the outward K+ channels (stomatal closure). 3. Hydrogen peroxide inhibits stomatal opening and induces stomatal closure in epidermal peels isolated from Vicia faba. 4. Hydrogen peroxide enhances stomatal closure by increasing K+ efflux from guard cells via outward rectifying K+ channels. 5. Based on epidermal peel experiments we have indirectly shown that Ca2+ may play a role in the guard cell response to O3. However, direct measurement of the guard cell [Ca2+]cyt did not show a response to O3. 6. Three Israeli cultivars of zucchini, Clarita, Yarden and Bareqet, were shown to be relatively sensitive to O3 (0.12 ml1-1 ). 7. Two environmentally important Israeli pine species are adversely affected by O3, even at 0.050 ml1-1 , a level frequently exceeded under local tropospheric conditions. P. brutia may be better equipped than P. halepensis to tolerate O3 stress. 8. Ozone directly affects pigment biosynthesis in pine seedlings, as well as the metabolism of O5 precursors, thus affecting the allocation of resources among various metabolic pathways. 9. Ozone induces activity of antioxidant enzymes, and of ascorbate content i the mesophyll and epidermis cells of Commelina communis L. Implications, both scientific and agricultural We have improved the understanding of how O3 and H2O2 do affect guard cell and stomatal function. We have shown that economical important Israeli species like zucchini and pine are relatively sensitive to O3.

Signalling gates in abscisic acid-mediated control of guard cell ion channels

1997 ◽  
Vol 100 (3) ◽  
pp. 481-490 ◽  
Author(s):  
Michael R. Blatt ◽  
Alexander Grabov
Keyword(s):  
Abscisic Acid ◽  
Ion Channels ◽  
Guard Cell

scholarly journals Postoperative malignant hyperthermia confirmed by calcium-induced calcium release rate after breast cancer surgery, in which prompt recognition and immediate dantrolene administration were life-saving: a case report

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Natsumi Miyazaki ◽  
Takayuki Kobayashi ◽  
Takako Komiya ◽  
Toshio Okada ◽  
Yusuke Ishida ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Body Temperature ◽  
Malignant Hyperthermia ◽  
Muscle Biopsy ◽  
Release Rate ◽  
Calcium Release ◽  
Cancer Surgery ◽  
Breast Cancer Surgery ◽  
Body Cooling ◽  
Calcium Induced Calcium Release

Abstract Background Malignant hyperthermia (MH) is a rare genetic disease characterized by the development of very serious symptoms, and hence prompt and appropriate treatment is required. However, postoperative MH is very rare, representing only 1.9% of cases as reported in the North American Malignant Hyperthermia Registry (NAMHR). We report a rare case of a patient who developed sudden postoperative hyperthermia after mastectomy, which was definitively diagnosed as MH by the calcium-induced calcium release rate (CICR) measurement test. Case presentation A 61-year-old Japanese woman with a history of stroke was hospitalized for breast cancer surgery. General anesthesia was introduced by propofol, remifentanil, and rocuronium. After intubation, anesthesia was maintained using propofol and remifentanil, and mastectomy and muscle flap reconstruction surgery was performed and completed without any major problems. After confirming her spontaneous breathing, sugammadex was administered and she was extubated. Thereafter, systemic shivering and masseter spasm appeared, and a rapid increase in body temperature (maximum: 38.9 °C) and end-tidal carbon dioxide (ETCO2) (maximum: 59 mmHg) was noted. We suspected MH and started cooling the body surface of the axilla, cervix, and body trunk, and administered chilled potassium-free fluid and dantrolene. After her body temperature dropped and her shivering improved, dantrolene administration was ended, and finally she was taken to the intensive care unit (ICU). Body cooling was continued within the target range of 36–37 °C in the ICU. No consciousness disorder, hypotension, increased serum potassium level, metabolic acidosis, or cola-colored urine was observed during her ICU stay. Subsequently, her general condition improved and she was discharged on day 12. Muscle biopsy after discharge was performed and provided a definitive diagnosis of MH. Conclusions The occurrence of MH can be life-threatening, but its frequency is very low, and genetic testing and muscle biopsy are required to confirm the diagnosis. On retrospective evaluation using the malignant hyperthermia scale, the present case was almost certainly that of a patient with MH. Prompt recognition and immediate treatment with dantrolene administration and body cooling effectively reversed a potentially fatal syndrome. This was hence a valuable case of a patient with postoperative MH that led to a confirmed diagnosis by CICR.

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