Low CO2 and stomata closure

 

 

 

Low carbon dioxide concentrations can reverse stomatal closure during water stress.

by Bunce J. A. (2007)

in  Physiol. Plant. 130, 552–559. doi: 10.1111/j.1399-3054.2007.00937.x –

CrossRef Full Text | Google Scholar

WEBSITE IS NOT AVAILABLE

 

 

Advertisements

K+ channels of stomatal guard cells

 

 

K+ channels of stomatal guard cells: abscisic acid evoked control of the outward rectifier mediated by cytoplasmic pH.

by Blatt M. R., Armstrong F. (1993)

in Planta, 191,330341. –

CrossRef |

http://link.springer.com/article/10.1007%2FBF00195690

Abstract

The activation by abscisic acid (ABA) of current through outward-rectifying K+ channels and its dependence on cytoplasmic pH (pHi) was examined in stomatal guard cells of Vicia faba L.

Intact guard cells were impaled with multibarrelled and H+-selective microelectrodes to record membrane potentials and pHi during exposures to ABA and the weak acid butyrate. Potassium channel currents were monitored under voltage clamp and, in some experiments, guard cells were loaded with pH buffers by iontophoresis to suppress changes in pHi. Following impalements, stable pHivalues ranged between 7.53 and 7.81 (7.67±0.04, n = 17). On adding 20 μM ABA, pHi rose over periods of 5–8 min to values 0.27±0.03 pH units above the pHi before ABA addition, and declined slowly thereafter.

Concurrent voltage-clamp measurements showed a parallel rise in the outward-rectifying K+ channel current (IK, out) and, once evoked, both pHi and IK, out responses were unaffected by ABA washout. Acid loads, imposed with external butyrate, abolished the ABA-evoked rise in IK, out. Butyrate concentrations of 10 and 30 mM (pH0 6.1) caused pHi to fall to values near 7.0 and below, both before and after adding ABA, consistent with a cytoplasmic buffer capacity of 128±12 mM per pH unit (n = 10) near neutrality.

Butyrate washout was characterised by an appreciable alkaline overshoot in pHi and concomitant swell in the steady-state conductance of IK, out. The rise in pHi and iK, out in ABA were also virtually eliminated when guard cells were first loaded with pH buffers to raise the cytoplasmic buffer capacity four- to sixfold; however, buffer loading was without appreciable effect on the ABA-evoked inactivation of a second, inward-rectifying class of K+ channels (IK, in).

The pHi dependence of IK, out was consistent with a cooperative binding of at least 2H+ (apparent pKa = 8.3) to achieve a voltage-independent block of the channel.

These results establish a causal link previously implicated between cytoplasmic alkalinisation and the activation of IK, out in ABA and, thus, affirm a role for H+ in signalling and transport control in plants distinct from its function as a substrate in H+-coupled transport. Additional evidence implicates a coordinate control of IK, in by cytoplasmic-free [Ca2+] and pHi.

Ion channel gating in plants

 

 

Ion channel gating in plants: physiological implications and integration for stomatal function.

Blatt M. R. (1991)

in  Journal of Membrane Biology 124: 95112. –

CrossRef |PubMed |CAS |

 

http://link.springer.com/article/10.1007%2FBF01870455

http://www.ncbi.nlm.nih.gov/pubmed/1662287

http://chemport.cas.org/cgi-bin/sdcgi?APP=ftslink&action=reflink&origin=wiley&version=1%2E0&coi=1%3aCAS%3a528%3aDyaK38Xjsl2jtA%253D%253D&md5=21cdf35c593345100f35905695984434

Guard cell sensing of rising CO2

 

 

The cellular basis of guard cell sensing of rising CO2.

by Assmann S. M. (1999)

in Plant, Cell & Environment 22: 629637. – DOI: 10.1046/j.1365-3040.1999.00408.x

Wiley Online Library |CAS |

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-3040.1999.00408.x/full

http://chemport.cas.org/cgi-bin/sdcgi?APP=ftslink&action=reflink&origin=wiley&version=1%2E0&coi=1%3aCAS%3a528%3aDyaK1MXksVartLg%253D&md5=dbae3e0956821e3457cdcde4f08deb06

Abstract

Numerous studies conducted on both whole plants and isolated epidermes have documented stomatal sensitivity to CO2. In general, CO2 concentrations below ambient stimulate stomatal opening, or an inhibition of stomatal closure, while CO2concentrations above ambient have the opposite effect.

The rise in atmospheric CO2 concentrations which has occurred since the industrial revolution, and which is predicted to continue, will therefore alter rates of transpirational water loss and CO2 uptake in terrestrial plants.

An understanding of the cellular basis for guard cell CO2 sensing could allow us to better predict, and perhaps ultimately to manipulate, such vegetation responses to climate change.

However, the mechanisms by which guard cells sense and respond to the CO2 signal remain unknown. It has been hypothesized that cytosolic pH and malate levels, cytosolic Ca2+ levels, chloroplastic zeaxanthin levels, or plasma-membrane anion channel regulation by apoplastic malate are involved in guard cell perception and response to CO2.

In this review, these hypotheses are discussed, and the evidence for guard cell acclimation to prevailing CO2 concentrations is also considered.

See the full article: Wiley Online Library

Ionic currents in guard cell vacuoles

 

 

Control of ionic currents in guard cell vacuoles by cytoplasmic and luminal calcium.

Allen G. J., Sanders D. (1996)

in Plant J., 10, 10551069. – DOI: 10.1046/j.1365-313X.1996.10061055.x

Wiley Online Library |PubMed |

http://onlinelibrary.wiley.com/doi/10.1046/j.1365-313X.1996.10061055.x/full

http://www.ncbi.nlm.nih.gov/pubmed/9011087

Abstract

Activity of vacuolar ion channels can be regulated by the cytosolic free Ca2+ concentration ([Ca2+]cyt). Using the whole-vacuole mode of patch-clamp with Vicia faba guard cell vacuoles, three distinct cation currents were apparent that were differentially regulated by [Ca2+]cyt. At ‘zero’ to 100 nM [Ca2+]cyt, instantaneous currents typical of Fast Vacuolar (FV) channels were activated. A 10 fold KCl gradient directed out of the vacuole increased FV currents (up to fivefold) at negative potentials compared with the currents in symmetrical KCl. At [Ca2+]cyt higher than 100 nM, instantaneous currents became smaller and voltage-independent (non-rectifying) and were typical of Vacuolar K,+-selective (VK) channels. These currents were less sensitive to a KCl gradient than were the FV currents, being stimulated less than twofold at negative potentials.

Reversal potentials measured in the presence of a KCl gradient indicated a high K+ permeability of both FV and VK currents. At [Ca2+]cyt higher than 600 nM time-dependent currents elicited by positive potentials were typical of SlowVacuolar (SV) channel activation.

When the Ca2+ mole fraction in the cytosolic or luminal solution was varied the reversal potential of SV currents (determined by tail current analysis) passed through maximum or minimum values. The resultant calculated apparent permeability ratios varied with ionic conditions but indicated high Ca2+ and K+ permeabilities. If a Cl permeability was assumed then the apparent PCa was lower. However, substitution of Cl by the larger (impermeant) anion gluconate had no effect on the reversal potential of SV tail currents in the presence of Ca2+ and a K+ gradient, demonstrating that the assumption of Cl permeability of the SV channel is invalid. Single-channel SV currents also decreased with increasing cytosolic Ca2+mole fraction.

These data indicate that the SV channel is highly cation selective, shows characteristics typical of a multi-ion pore and derives ion selectivity by Ca2+ binding. The SV channel currents could also be Mg2+-activated and were demonstrated to be Mg2+-permeable in the absence of Ca2+. The apparent permeability ratio (PMg:PK) also varied under different ionic conditions.

The results indicate not only that FV, VK and SV channels are all present in a single cell type, but also that each is differentially regulated by [Ca2+]cyt. The respective roles of these channels in vacuolar ion release are discussed, and possible conditions are presented in which these channels could be activated by disparate signalling pathways during stomatal closure.

ABA-induced cytoplasmic calcium rises in stomata

 

 

Arabidopsis abi1-1 and abi2-1 phosphatase mutations reduce abscisic acid-induced cytoplasmic calcium rises in guard cells.

by Allen G. J., Kuchitsu K., Chu S. P., Murata Y., Schroeder J. I. (1999)

in  Plant Cell 11: 1785–1798 – 

CrossRef |PubMed |

http://www.plantcell.org/content/11/9/1785

http://www.ncbi.nlm.nih.gov/pubmed/10488243

 

Abstract

Elevations in cytoplasmic calcium ([Ca(2)+](cyt)) are an important component of early abscisic acid (ABA) signal transduction. To determine whether defined mutations in ABA signal transduction affect [Ca(2)+](cyt) signaling, the Ca(2)+-sensitive fluorescent dye fura 2 was loaded into the cytoplasm of Arabidopsis guard cells. Oscillations in [Ca(2)+](cyt) could be induced when the external calcium concentration was increased, showing viable Ca(2)+ homeostasis in these dye-loaded cells. ABA-induced [Ca(2)+](cyt) elevations in wild-type stomata were either transient or sustained, with a mean increase of approximately 300 nM.

Interestingly, ABA-induced [Ca(2)+](cyt) increases were significantly reduced but not abolished in guard cells of the ABA-insensitive protein phosphatase mutants abi1 and abi2.

Plasma membrane slow anion currents were activated in wild-type, abi1, and abi2 guard cell protoplasts by increasing [Ca(2)+](cyt), demonstrating that the impairment in ABA activation of anion currents in the abi1 and abi2 mutants was bypassed by increasing [Ca(2)+](cyt).

Furthermore, increases in external calcium alone (which elevate [Ca(2)+](cyt)) resulted in stomatal closing to the same extent in the abi1 and abi2 mutants as in the wild type.

Conversely, stomatal opening assays indicated different interactions of abi1 and abi2, with Ca(2)+-dependent signal transduction pathways controlling stomatal closing versus stomatal opening.

Together, [Ca(2)+](cyt) recordings, anion current activation, and stomatal closing assays demonstrate that the abi1 and abi2 mutations impair early ABA signaling events in guard cells upstream or close to ABA-induced [Ca(2)+](cyt) elevations.

These results further demonstrate that the mutations can be bypassed during anion channel activation and stomatal closing by experimental elevation of [Ca(2)+](cyt).

Stimulus-specific calcium oscillations are necessary for stomatal closure

 

 

Alteration of stimulus-specific guard cell calcium oscillations and stomatal closing in Arabidopsis det3mutant.

by Allen G. J., Chu S. P., Schumacher K., Shimazaki C. T., Vafeados D., Kemper A., Hawke S. D.Tallman G., Tsien R. Y., Harper J. F., Chory J., Schroeder J. I. (2000)

in Science 289: 23382342. –

CrossRef |PubMed |CAS |

http://science.sciencemag.org/content/289/5488/2338

http://www.ncbi.nlm.nih.gov/pubmed/11009417

http://chemport.cas.org/cgi-bin/sdcgi?APP=ftslink&action=reflink&origin=wiley&version=1%2E0&coi=1%3aCAS%3a528%3aDC%252BD3cXmvF2ru7o%253D&md5=a8bfed4c1553f06ca3e2a9ffe30a9447

Abstract

Cytosolic calcium oscillations control signaling in animal cells, whereas in plants their importance remains largely unknown. In wild-type Arabidopsis guard cells abscisic acid, oxidative stress, cold, and external calcium elicited cytosolic calcium oscillations of differing amplitudes and frequencies and induced stomatal closure.

In guard cells of the V-ATPase mutant det3, external calcium and oxidative stress elicited prolonged calcium increases, which did not oscillate, and stomatal closure was abolished.

Conversely, cold and abscisic acid elicited calcium oscillations in det3, and stomatal closure occurred normally. Moreover, in det3 guard cells, experimentally imposing external calcium-induced oscillations rescued stomatal closure.

These data provide genetic evidence that stimulus-specific calcium oscillations are necessary for stomatal closure.