The effects of ABA on channel-mediated K(+) transport across higher plant roots.
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The transport and accumulation of K(+) in higher plant roots is regulated by ABA. Molecular and electrophysiological techniques have identified a number of discrete transporters which are involved in the translocation of K(+) from the soil solution to the shoots of higher plants. Furthermore, recent reports have shown that ABA regulates K(+) channel activity in maize and Arabidopsis roots which suggests that ABA regulation of K(+) transport in roots is, at least in part, ion channel-mediated. The signalling processes which underlie the ABA regulation of K(+) channels have been investigated. The effects of ABA on the membrane potential of intact maize root cells were also studied. It was found that ABA regulated the membrane potential of root cells and that this regulation is consistent with the hypothesis that ABA-induced K(+) accumulation in roots is mediated by K(+) channels. (+info)
Alteration of stimulus-specific guard cell calcium oscillations and stomatal closing in Arabidopsis det3 mutant.
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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. (+info)
ABA activates multiple Ca(2+) fluxes in stomatal guard cells, triggering vacuolar K(+)(Rb(+)) release.
(51/1560)
The mechanisms by which abscisic acid (ABA) activates the release of K(+)(Rb(+)) from the vacuole of stomatal guard cells, a process essential for ABA-induced stomatal closure, have been investigated by tracer flux measurements. The form and timing of the ABA-induced efflux transient could be manipulated by treatments that alter three potential Ca(2+) fluxes into the cytoplasm, the influx from the outside and two pathways of internal release, those dependent on phospholipase C (inhibited by ) and cyclic ADP-ribose (inhibited by nicotinamide). Ba(2+), acting as a competitive inhibitor of Ca(2+) influx but also as an inhibitor of internal release, was an effective inhibitor of the transient. The results suggest that a threshold level of cytoplasmic Ca(2+) is required for the initiation of the minimal efflux transient after a lag period and with a low rate of rise. As conditions improve for the generation of an efflux transient (higher ABA or reduced Ba(2+)), a second threshold is crossed, generating a transient with zero lag and rapid rate of rise. This may reflect different Ca(2+) levels required for activation of different tonoplast K(+) channels. In this state, at high ABA, the transient is inhibited by removal of external Ca(2+), suggesting Ca(2+) influx makes a major contribution to increase in cytoplasmic Ca(2+). By contrast, at low ABA, the transient is not inhibited by removal of external Ca(2+) but is sensitive to either or nicotinamide, suggesting internal release makes the major contribution, involving both pathways. ABA appears to activate all three processes, and their relative importance depends on conditions. (+info)
Abscisic acid stimulation of phospholipase D in the barley aleurone is G-protein-mediated and localized to the plasma membrane.
(52/1560)
We have previously determined that phospholipase D (PLD) is activated by abscisic acid (ABA), and this activation is required for the ABA response of the cereal aleurone cell. In this study, ABA-stimulated PLD activity was reconstituted in vitro in microsomal membranes prepared from aleurone protoplasts. The transient nature (20 min) and degree (1.5- to 2-fold) of activation in vitro were similar to that measured in vivo. Stimulation by ABA was only apparent in the membrane fraction and was associated with a fraction enriched in plasma membrane. These results suggest that an ABA receptor system and elements linking it to PLD activation are associated with the aleurone plasma membrane. The activation of PLD in vitro by ABA was dependent on the presence of GTP. Addition of GTPgammaS transiently stimulated PLD in an ABA-independent manner, whereas treatment with GDPbetaS or pertussis toxin blocked the PLD activation by ABA. Application of pertussis toxin to intact aleurone protoplasts inhibited the ability of ABA to activate PLD as well as antagonizing the ability of ABA to down-regulate gibberellic acid-stimulated alpha-amylase production. All of these data support the hypothesis that ABA stimulation of PLD activity occurs at the plasma membrane and is mediated by G-protein activity. (+info)
Differential effects of methyl jasmonate on the expression of the early light-inducible proteins and other light-regulated genes in barley.
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The effects of methyl jasmonate (JA-Me) on early light-inducible protein (ELIP) expression in barley (Hordeum vulgare L. cv Apex) have been studied. Treatment of leaf segments with JA-Me induces the same symptoms as those exhibited by norflurazon bleaching, including a loss of pigments and enhanced light stress that results in increased ELIP expression under both high- and low-light conditions. The expression of both low- and high-molecular-mass ELIP families is considerably down-regulated by JA-Me at the transcript and protein levels. This repression occurs despite increased photoinhibition measurable as a massive degradation of D1 protein and a delayed recovery of photosystem II activity. In JA-Me-treated leaf segments, the decrease of the photochemical efficiency of photosystem II under high light is substantially more pronounced as compared to controls in water. The repression of ELIP expression by JA-Me is superimposed on the effect of the increased light stress that leads to enhanced ELIP expression. The fact that the reduction of ELIP transcript levels is less pronounced than those of light-harvesting complex II and small subunit of Rubisco transcripts indicates that light stress is still affecting gene expression in the presence of JA-Me. The jasmonate-induced protein transcript levels that are induced by JA-Me decline under light stress conditions. (+info)
Abscisic acid plasmalemma perception triggers a calcium influx essential for RAB18 gene expression in Arabidopsis thaliana suspension cells.
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Pretreatment of Arabidopsis thaliana suspension cells with impermeant calcium chelator EGTA inhibited the ABA-induced RAB18 gene expression. However, extracellular calcium alone, up to 10 mM, did not trigger RAB18 expression. Spectrofluorimetric extracellular Ca(2+) measurement with Fluo-3 showed a fast, within 1 min, Ca(2+) influx associated with outer plasmalemma ABA perception. In the presence of the Ca(2+) blockers Cd(2+) and Ni(2+), RAB18 expression was suppressed. Pimozide and fluspirilene inhibited Ca(2+) influx and ABA-induced RAB18 expression. Thus we demonstrated the involvement of specific Ca(2+) influx in the ABA signaling sequence leading to RAB18 expression. (+info)
The Arabidopsis aldehyde oxidase 3 (AAO3) gene product catalyzes the final step in abscisic acid biosynthesis in leaves.
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Abscisic acid (ABA) is a plant hormone involved in seed development and germination and in responses to various environmental stresses. The last step of ABA biosynthesis involves oxidation of abscisic aldehyde, and aldehyde oxidase (EC ) is thought to catalyze this reaction. An aldehyde oxidase isoform, AOdelta, encoded by AAO3, one of four Arabidopsis aldehyde oxidase genes (AAO1, AAO2, AAO3, and AAO4), is the most likely candidate for the enzyme, because it can efficiently catalyze the oxidation of abscisic aldehyde to ABA. Here, we report the isolation and characterization of an ABA-deficient Arabidopsis mutant that maps at the AAO3 locus. The mutant exhibits a wilty phenotype in rosette leaves, but seed dormancy is not affected. ABA levels were significantly reduced in the mutant leaves, explaining the wilty phenotype in rosettes, whereas the level in the mutant seeds was less reduced. No AOdelta activity could be detected in the rosette leaves of the mutant. Sequence data showed that the mutant contains a G to A substitution in the AAO3 gene. The mutation causes incorrect splicing of the ninth intron of AAO3 mRNA. We thus conclude that the ABA-deficient mutant is impaired in the AAO3 gene and that the gene product, AOdelta, is an aldehyde oxidase that catalyzes the last step of ABA biosynthesis in Arabidopsis, specifically in rosette leaves. Other aldehyde oxidases may be involved in ABA biosynthesis in other organs. (+info)
Inactivation of a MAPK-like protein kinase and activation of a MBP kinase in germinating barley embryos.
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We provide evidence for involvement of two different 45 kDa protein kinases in rehydration and germination of barley embryos. In dry embryos, a myelin basic protein (MBP) phosphorylating kinase was detected, which could be immunoprecipitated with an anti-MAPK (mitogen-activated protein kinase) antibody. Rehydration of the embryo induced a decrease in activity of this 45 kDa MAPK-like protein kinase. In addition, activity of a MBP kinase of the same molecular weight was subsequently found to be induced. This second MBP kinase activity could not be immunoprecipitated with the anti-MAPK antibody and was induced only in germinating embryos, not in dormant embryos. (+info)