共查询到20条相似文献,搜索用时 31 毫秒
1.
To determine whether Ca 2+ plays a special role in the early graviresponse of shoots, as has been reported for roots, we treated etiolated pea epicotyls with substances known to antagonize Ca 2+ (La 3+), to remove Ca 2+ from the wall (spermidine, EGTA), to inhibit calmodulin mediated reactions (chlorpromazine), or to inhibit IAA transport (TIBA). We studied the effect of these substances on IAA and Ca 2+ uptake into 7 mm long subapical 3rd internode etiolated pea epicotyl sections and pea leaf protoplasts, on pea epicotyl growth, and graviresponse and on lateral IAA redistribution during gravistimulation.Our results support the view that adequate Ca 2+ in the apoplast is required for normal IAA uptake, transport and graviresponse. Experiments with protoplasts indicate that Ca 2+ may be controlling a labile membrane porter, possibly located on the external surface of cell membrane, while inhibitor experiments suggest that calmodulin is also implicated in both the movement of IAA and graviresponse. Since a major transfer of Ca 2+ through free space during graviresponse has not yet been demonstrated, and since inhibition of calcium channels does not affect IAA redistribution (Migliaccio and Galston, 1987, Plant Physiology 85:542), we conclude that no clear evidence links prior Ca 2+ movement with IAA redistribution during graviresponse in stems.Abbreviations IAA
indole-3-acetic acid
- CPZ
chlorpromazine
- EGTA
ethylene glycol bis-(aminoethyl ether) N, N, N 1, N 1-tetracetic acid
- G C
gravicurvature
The research was supported by NASA grant NSG-7290 to AWG. 相似文献
2.
The capacity of excised internode sections of pea to grow and secrete protons in response to indoleacetic acid (IAA) and Ca 2+ and K + treatments was examined. By incubating unpeeled and unabraded sections in rapidly flowing solutions, it was shown that acidification of the external medium in the presence or absence of IAA is dependent on the presence of Ca 2+ and K +. Similar results were obtained when unpeeled and unabraded sections were incubated in dishes with shaking. When peeled or abraded sections were incubated with shaking in IAA, H + release was also dependent on the presence of Ca 2+ and K +. The release of H + from sections incubated in Ca 2+ and K + is not caused by displacement of H + from binding sites in the cell wall. Rather, the release of protons from sections is temperature dependent, and it is concluded that this is a metabolically linked process. Although Ca 2+ and K + are essential for the release of H + from isolated stem sections of peas, these cations do not influence elongation. Despite the large increase in proton release induced by Ca 2+ and K + either in the presence or absence of auxin, growth in the presence of these ions was never greater than it was in their absence. Furthermore, cations do not affect the neutral sugar or uronic acid composition of the solution which can be centrifuged from isolated sections. As is the case for growth, an increase in the neutral sugar and uronide composition of the cell wall solution is dependent only on IAA. It is concluded that IAA-induced growth of pea stem sections is independent of the secretion of protons. 相似文献
3.
During the ascidian sperm reaction the single large cylindrical mitochondrion which lies next to the nucleus in the head swells, becomes spherical, and migrates along the tail to be lost when it reaches the end. This sequence is initiated by eggs, egg water, high pH, low Na +, or the ionophore X537A. Accompanying the sperm reaction induced by low Na + are H + efflux and Ca 2+ influx in a ratio of near 100:1 as determined by 45Ca 2+ and atomic absorption analysis. Simultaneous pH and Ca 2+ electrode measurements suggest that the movement of H + begins 10–13 sec before the movement of Ca 2+. Ca 2+ uptake can be inhibited by verapamil without affecting H + efflux or the sperm reaction. Acid release and Ca 2+ uptake are proportional to the initial pH of the medium when the reaction is triggered by high pH. Acid release initiated by low Na + is proportional to Ca 2+ concentrations above 2 m M. H + and Ca 2+ movements differ in magnitude, kinetics, and inhibition by verapamil, thus suggesting that H + is probably not exchanged for Ca 2+. Instead we propose that loss of H + triggers the uptake of Ca 2+, which initiates the sperm reaction. 相似文献
4.
Bongkrekic acid and atractyloside, inhibitors of adenine nucleotide translocase, do not inhibit Ca 2+ uptake and H + production by pig heart mitochondria. However, bongkrekic acid, but not atractyloside, inhibits dinitrophenol-induced Ca 2+ efflux and H + uptake. Conversely, ruthenium red blocks Ca 2+ uptake and H + production but does not prevent dinitrophenol-induced Ca 2+ efflux and H + uptake by mitochondria. These results suggest that mitochondrial Ca 2+ uptake and release exist as two independent pathways. The efflux of Ca 2+ from mitochondria is mediated by a bongkrekic acid sensitive component which is apparently not identical to the ruthenium red sensitive Ca 2+ uptake carrier. 相似文献
6.
Microsomal vesicles from 24-hour-old radish ( Raphanus sativus L.) seedlings accumulate Ca 2+ upon addition of MgATP. MgATP-dependent Ca 2+ uptake co-migrates with the plasma membrane H +-ATPase on a sucrose gradient. Ca 2+ uptake is insensitive to oligomycin, inhibited by vanadate (IC 50 40 micromolar) and erythrosin B (IC 50 0.2 micromolar) and displays a pH optimum between pH 6.6 and 6.9. MgATP-dependent Ca 2+ uptake is insensitive to protonophores. These results indicate that Ca 2+ transport in these microsomal vesicles is catalyzed by a Mg 2+-dependent ATPase localized on the plasma membrane. Ca 2+ strongly reduces ΔpH generation by the plasma membrane H +-ATPase and increases MgATP-dependent membrane potential difference (Δψ) generation. These effects of Ca 2+ on ΔpH and Δψ generation are drastically reduced by micromolar erythrosin B, indicating that they are primarily a consequence of Ca 2+ uptake into plasma membrane vesicles. The Ca 2+-induced increase of Δψ is collapsed by permeant anions, which do not affect Ca 2+-induced decrease of ΔpH generation by the plasma membrane H +-ATPase. The rate of decay of MgATP-dependent ΔpH, upon inhibition of the plasma membrane H +-ATPase, is accelerated by MgATP-dependent Ca 2+ uptake, indicating that the decrease of ΔpH generation induced by Ca 2+ reflects the efflux of H + coupled to Ca 2+ uptake into plasma membrane vesicles. It is therefore proposed that Ca 2+ transport at the plasma membrane is mediated by a Mg 2+-dependent ATPase which catalyzes a nH +/Ca 2+ exchange. 相似文献
7.
Mitochondria from some plant tissues possess the ability to take up Ca 2+ by a phosphate-dependent mechanism associated with a decrease in membrane potential, H + extrusion, and increase in the rate of respiration (AE Vercesi, L Pereira da Silva, IS Martins, CF Bernardes, EGS Carnieri, MM Fagian [1989] In G Fiskum, ed, Cell Calcium Metabolism. Plenum Press, New York, pp 103-111). The present study reexamined the nature of the phosphate requirement in this process. The main observations are: (a) Respiration-coupled Ca 2+ uptake by isolated corn ( Zea mays var Maya Normal) mitochondria or carbonyl cyanide p-trifluoromethoxyphenylhydrazone-induced efflux of the cation from such mitochondria are sensitive to mersalyl and cannot be dissociated from the silmultaneous movement of phosphate in the same direction. (b) Ruthenium red-induced efflux is not affected by mersalyl and can occur in the absence of phosphate movement. (c) In Ca 2+-loaded corn mitochondria, mersalyl causes net Ca 2+ release unrelated to a decrease in membrane potential, probably due to an inhibition of Ca 2+ cycling at the level of the influx pathway. It is concluded that corn mitochondria (and probably other plant mitochondria) do possess an electrophoretic influx pathway that appears to be a mersalyl-sensitive Ca 2+/inorganic phosphate-symporter and a phosphate-independent efflux pathway possibly similar to the Na 2+-independent Ca 2+ efflux mechanism of vertebrate mitochondria, because it is not stimulated by Na +. 相似文献
8.
The release of H + during the oxalate-supported Ca 2+ uptake in sarcoplasmic reticulum vesicles is kinetically coincident with the initial phase of Ca 2+ accumulation. The Ca 2+ uptake is increased and the H + release is decreased in the presence of KCl and other monovalent chloride salts as expected for a H +-monovalent cation exchange. The functioning of the Ca 2+-pump is disturbed by the presence of potassium gluconate and, to a lesser extent, of choline chloride. These salts do not inhibit the ATPase activity of Ca 2+-permeable vesicles, suggesting a charge imbalance inhibition which is specially relevant in the case of gluconate. Therefore, K +, and also Cl –, appear to be involved in secondary fluxes during the active accumulation of Ca 2+. The microsomal preparation seems homogeneous with respect to the K +-channel, showing an apparent rate constant for K + release of approximately 25 s –1 measured with the aid of 86Rb + tracer under equilibrium conditions. A Rb + efflux, sensitive to Ca 2+-ionophore, can be also detected during the active accumulation of Ca 2+. The experimental data suggest that both monovalent cations and anions are involved in a charge compensation during the Ca 2+ uptake and H + release. Fluxes of these highly permeable ions would contribute to cancel the formation of a resting membrane potential through the sarcoplasmic reticulum membrane. 相似文献
9.
The mechanisms by which cationic amino acids influence pancreatic B-cell function have been studied by monitoring simultaneously 86Rb + efflux and insulin release from perifused rat islets. The effects of two reference amino acids arginine and lysine were compared with those of closely related substances to define the structural requirements for recognition of these molecules as secretagogues. Arginine accelerated 86Rb + efflux and increased insulin release in the absence or in the presence of 7m m-glucose. Its effects on efflux did not require the presence of extracellular Ca 2+ or Na +, but its insulinotropic effects were suppressed in a Ca 2+-free medium and inhibited in an Na +-free medium. Among arginine derivatives, only 2-amino-3-guanidinopropionic acid mimicked its effects on 86Rb + efflux and insulin release; citrulline, guanidinoacetic acid, 3-guanidinopropionic acid and guanidine were inactive. Norvaline and valine also increased 86Rb + efflux, but their effect required the presence of extracellular Na +; they did not stimulate insulin release. Lysine as well as the shorter-chain cationic amino acids ornithine and 2,4-diaminobutyric acid accelerated 86Rb + efflux in a Ca 2+- and Na +-independent manner. Their stimulation of insulin release was suppressed by Ca 2+ omission, but only partially inhibited in an Na +-free medium. The uncharged glutamine and norleucine increased the rate of 86Rb + efflux in the presence of glucose, only if extracellular Na + was present. Norleucine slightly increased release in a Ca 2+- and Na +-dependent manner. The effects of lysine on efflux and release were not mimicked by other related substances such as 1,5-diaminopentane and 6-aminohexanoic acid. The results suggest that the depolarizing effect of cationic amino acids is due to accumulation of these positively charged molecules in B-cells. This causes acceleration of the efflux of K + ( 86Rb +) and activation of the influx of Ca 2+ (which triggers insulin release). The prerequisite for the stimulation of B-cells by this mechanism appears to be the presence of a positive charge on the side chain of the amino acid, rather than a specific group. 相似文献
10.
A rapid loss of accumulated Ca 2+ is produced by addition of H + to isolated heart mitochondria. The H +-dependent Ca + efflux requires that either (a) the NAD(P)H pool of the mitochondrion be oxidized, or (b) the endogenous adenine nucleotides be depleted. The loss of Ca 2+ is accompanied by swelling and loss of endogenous Mg 2–. The rate of H +-dependent Ca 2+ efflux depends on the amount of Ca 2+ and P i taken up and the extent of the pH drop imposed. In the absence of ruthenium red the H +-induced Ca 2+-efflux is partially offset by a spontaneous re-accumulation of released Ca 2+. The H +-induced Ca 2+ efflux is inhibited when the P i transporter is blocked with N-ethylmaleimide, is strongly opposed by oligomycin and exogenous adenine nucleotides (particularly ADP), and inhibited by nupercaine. The H +-dependent Ca 2+ efflux is decreased markedly when Na + replaces the K + of the suspending medium or when the exogenous K +/H + exchanger nigericin is present. These results suggest that the H +-dependent loss of accumulated Ca 2+ results from relatively nonspecific changes in membrane permeability and is not a reflection of a Ca 2+/H + exchange reaction. 相似文献
11.
Phosphoenolpyruvate was found to depress extra oxygen consumption associated with Ca 2+-induced respiratory jump by rat heart mitochondria. Addition of phosphoenolpyruvate to mitochondria which have accumulated Ca 2+ in the presence of glutamate and inorganic phosphate causes the release of Ca 2+ from mitochondria. The phosphoenolpyruvate-stimulated Ca 2+ efflux can be observed with mitochondria loaded with low initial Ca 2+ concentration (0.12 mM) in the incubation medium. Measurements of mitochondrial H + translocation produced by addition of Ca 2+ to respiring mitochondria show that phosphoenolpyruvate depresses H + ejection and enhances H + uptake by mitochondria. The Ca 2+-releasing effect of phosphoenolpyruvate was found to be significantly stronger than that produced by rotenone when added to mitochondria loaded with Ca 2+ in the presence of glutamate and inorganic phosphate. Dithiothreitol cannot overcome the effect of phosphoenolpyruvate on mitochondrial Ca 2+ transport. 相似文献
12.
Calcium flux in sunflower ( Helianthus annuus L. cv Russian mammoth) hypocotyl was measured with a Ca 2+ electrode as the increase or decrease in Ca 2+ in an aqueous solution (10 micromolar CaCl 2) in contact with either the basal or apical end of 20 millimeter segments. Ca 2+ efflux was significantly higher at the apical end compared with the basal end; this apparent polarity was maintained even when the segments were inverted. No significant difference was observed in the cation exchange capacity of apical and basal cell walls that could explain the difference in Ca 2+ efflux at opposite ends of the hypocotyl segment. The presence of exogenous indoleacetic acid (IAA) in the segment medium resulted in the promotion of both Ca 2+ efflux and segment elongation. However, osmotic inhibition of the IAA-induced elongation did not result in inhibiting the IAA-induced Ca 2+ efflux. Ca 2+ efflux was inhibited by cyanide. Lowering the temperature from 25°C also caused the gradual reduction of Ca 2+ efflux; at 5°C the hypocotyl segments showed a net absorption of Ca 2+ from the segment medium. These findings support the suggestion that: (a) the observed Ca 2+ efflux in hypocotyl segments is probably the manifestation of the system which maintains the transmembrane Ca 2+ gradient at the cellular level. (b) The acropetal polarity of Ca 2+ efflux may be the result of the involvement of Ca 2+ in the basipetal transport of IAA. 相似文献
13.
Abstract: The features of Ca 2+ fluxes, the importance of the Ca 2+ pump‐mediated H +/Ca 2+ exchanges at plasmalemma level, and the possible involvement of Ca 2+‐ATPase activity in ABA‐induced changes of H + fluxes were studied in Egeria densa leaves. The results presented show that, while in basal conditions no net Ca 2+ flux was evident, a conspicuous Ca 2+ influx (about 1.1 ìmol g ?1 FW h ?1) occurred. The concomitant efflux of Ca 2+ was markedly reduced by treatment with 5 íM eosin Y (EY), a specific inhibitor of the Ca 2+‐ATPase, that completely blocked the transport of Ca 2+ after the first 20 ‐ 30 min. The decrease in Ca 2+ efflux induced by EY was associated with a significant increase in net H + extrusion (?ÄH +) and a small but significant cytoplasmic alkalinization. The shift of external [Ca 2+] from 0.3 to 0.2 mM (reducing Ca 2+ uptake by about 30 %) and the hindrance of Ca 2+ influx by La 3+ were accompanied by progressively higher ?ÄH + increases, in agreement with a gradual decrease in the activity of a mechanism counteracting the Ca 2+ influx by an nH +/Ca 2+ exchange. The ABA‐induced decreases in ?ÄH + and pH cyt were accompanied by a significant increase in Ca 2+ efflux, all these effects being almost completely suppressed by EY, in line with the view that the ABA effects on H + fluxes are due to activation of the plasmalemma Ca 2+‐ATPase. These results substantially stress the high sensitivity and efficacy of the plasmalemma Ca 2+ pump in removing from the cytoplasm the Ca 2+ taken up, and the importance of the contribution of Ca 2+ pump‐mediated H +/Ca 2+ fluxes in bringing about global changes of H + fluxes at plasmalemma level. 相似文献
14.
Net fluxes of Ca 2+, H + and K + were measured from intact Chara australis cells and from isolated cell walls, using ion-selective microelectrodes. In both systems, a stimulation in Ca 2+ efflux (up to 100 nmol m ?2 s ?1, from an influx of ~40 nmol m ?2 s ?1) was detected as the H + or K + concentration was progressively increased in the bathing solution (pH 7.0 to 4.6 or K + 0.2 to 10mol m ?3, respectively). A Ca 2+ influx of similar size occurred following the reverse changes. These fluxes decayed exponentially with a time constant of about 10 min. The threshold pH for Ca 2+ efflux (pH 5.2) is similar to a reported pH threshold for acid-induced wall extensibility in a closely related characean species. Application of NH 4+ to intact cells caused prolonged H + efflux and also transient Ca 2+ efflux. We attribute all these net Ca 2+ fluxes to exchange in the wall with H + or K +. A theoretical treatment of the cell wall ion exchanges, using the ‘weak acid Donnan Manning’ (WADM) model, is given and it agrees well with the data. The role of Ca 2+ in the cell wall and the effect of Ca 2+ exchanges on the measured fluxes of other ions, including bathing medium acidification by H + efflux, are discussed. 相似文献
15.
A transient Ca 2+ release from preloaded mitochondria can be induced by a sudden decrease in the pH of the outer medium from 8.0 or 7.4 to 6.8. In the presence of inorganic phosphate the released Ca 2+ is not taken up again. Upon Ca 2+ addition to respiring mitochondria the mitochondrial membrane potential (Δ♀) decreases to a new resting level. A further decrease in Δ♀ occurs after the decrease in pH from 7.4 to 6.8, concomitant with the reuptake phase of the Ca 2+ release. Phosphate, EGTA, and ruthenium red restore Δ♀ to its initial level. If phosphate is present initially, only transient changes in Δ♀ occur upon addition of Ca 2+ or H + ions. Only a small transient change in Δ♀ upon H + ion addition is seen in the absence of accumulated Ca 2+. La 3+, a competitive inhibitor of Ca 2+ transport, prevents the H + ion-induced Ca 2+ efflux, whereas this is not the case in the presence of the noncompetitive inhibitor ruthenium red. Ruthenium red, however, prevents the reuptake phase. Mg 2+, an inhibitor of the surface binding of Ca 2+, has no or only a slight effect on the H + ion-induced Ca 2+ release. Mitochondria preloaded with Ca 2+ release a small fraction of Ca 2+ during the subsequent uptake of another pulse of Ca 2+. The results indicate that at least one pool of mitochondrial Ca 2+ exists in a mobile state. The possible existence of a exchanger in the mitochondrial membrane is discussed. 相似文献
16.
High environmental salt elicits an increase in cytosolic Ca 2+ ([Ca 2+] cyt) in plants, which is generated by extracellular Ca 2+ influx and Ca 2+ release from intracellular stores, such as vacuole and endoplasmic reticulum. This study aimed to determine the physiological mechanisms underlying Ca 2+ release from vacuoles and its role in ionic homeostasis in Populus euphratica. In vivo Ca 2+ imaging showed that NaCl treatment induced a rapid elevation in [Ca 2+] cyt, which was accompanied by a subsequent release of vacuolar Ca 2+. In cell cultures, NaCl-altered intracellular Ca 2+ mobilization was abolished by antagonists of inositol (1, 4, 5) trisphosphate (IP 3) and cyclic adenosine diphosphate ribose (cADPR) signaling pathways, but not by slow vacuolar (SV) channel blockers. Furthermore, the NaCl-induced vacuolar Ca 2+ release was dependent on extracellular ATP, extracellular Ca 2+ influx, H 2O 2, and NO. In vitro Ca 2+ flux recordings confirmed that IP 3, cADPR, and Ca 2+ induced substantial Ca 2+ efflux from intact vacuoles, but this vacuolar Ca 2+ flux did not directly respond to ATP, H 2O 2, or NO. Moreover, the IP 3/cADPR-mediated vacuolar Ca 2+ release enhanced the expression of salt-responsive genes that regulated a wide range of cellular processes required for ion homeostasis, including cytosolic K + maintenance, Na + and Cl − exclusion across the plasma membrane, and Na +/H + and Cl −/H + exchanges across the vacuolar membrane. 相似文献
17.
Methyl jasmonate (MeJA) elicits stomatal closure in many plant species. Stomatal closure is accompanied by large ion fluxes across the plasma membrane (PM). Here, we recorded the transmembrane ion fluxes of H +, Ca 2+ and K + in guard cells of wild‐type (Col‐0) Arabidopsis, the CORONATINE INSENSITIVE1 ( COI1) mutant coi1‐1 and the PM H +‐ATPase mutants aha1‐6 and aha1‐7, using a non‐invasive micro‐test technique. We showed that MeJA induced transmembrane H + efflux, Ca 2+ influx and K + efflux across the PM of Col‐0 guard cells. However, this ion transport was abolished in coi1‐1 guard cells, suggesting that MeJA‐induced transmembrane ion flux requires COI1. Furthermore, the H + efflux and Ca 2+ influx in Col‐0 guard cells was impaired by vanadate pre‐treatment or PM H +‐ATPase mutation, suggesting that the rapid H + efflux mediated by PM H +‐ATPases could function upstream of the Ca 2+ flux. After the rapid H + efflux, the Col‐0 guard cells had a longer oscillation period than before MeJA treatment, indicating that the activity of the PM H +‐ATPase was reduced. Finally, the elevation of cytosolic Ca 2+ concentration and the depolarized PM drive the efflux of K + from the cell, resulting in loss of turgor and closure of the stomata. 相似文献
18.
The vacuolar pH and the trans-tonoplast ΔpH modifications induced by the activity of the two proton pumps H +-ATPase and H +-PPase and by the proton exchanges catalyzed by the Na +/H + and Ca 2+/H + antiports at the tonoplast of isolated intact vacuoles prepared from Catharanthus roseus cells enriched in inorganic phosphate (Y Mathieu et al 1988 Plant Physiol [in press]) were measured using the 31P NMR technique. The H +-ATPase induced an intravacuolar acidification as large as 0.8 pH unit, building a trans-tonoplast ΔpH up to 2.2 pH units. The hydrolysis of the phosphorylated substrate and the vacuolar acidification were monitored simultaneously to estimate kinetically the apparent stoichiometry between the vectorial proton pumping and the hydrolytic activity of the H +-ATPase. A ratio of H + translocated/ATP hydrolyzed of 1.97 ± 0.06 (mean ± standard error) was calculated. Pyrophosphate-treated vacuoles were also acidified to a significant extent. The H +-PPase at 2 millimolar PPi displayed hydrolytic and vectorial activities comparable to those of the H +-ATPase, building a steady state ΔpH of 2.1 pH units. Vacuoles incubated in the presence of 10 millimolar Na + were alkalinized by 0.4 to 0.8 pH unit. It has been shown by using 23Na NMR that sodium uptake was coupled to the H + efflux and occurred against rather large concentration gradients. For the first time, the activity of the Ca 2+/H + antiport has been measured on isolated intact vacuoles. Ca 2+ uptake was strongly inhibited by NH 4Cl or gramicidin. Vacuoles incubated with 1 millimolar Ca 2+ were alkalinized by about 0.6 pH unit and this H + efflux was associated to a Ca 2+ uptake as demonstrated by measuring the external Ca 2+ concentration with a calcium specific electrode. Steady state accumulation ratios of Ca 2+ as high as 100 were reached for steady state external concentrations about 200 micromolar. The rate of Ca 2+ uptake appeared markedly amplified in intact vacuoles when compared to tonoplast vesicles but the antiport displayed a much lower affinity for calcium. The different behavior of intact vacuoles compared to vesicles appears mainly to be due to differences in the surface to volume ratio and in the rates of dissipation of the pH gradient. Despite its low affinity, the Ca 2+/H + antiport has a high potential capacity to regulate cytoplasmic concentration of calcium. 相似文献
19.
Calcium transport into tomato ( Lycopersicon esculentum Mill, cv Castlemart) fruit tonoplast vesicles was studied. Calcium uptake was stimulated approximately 10-fold by MgATP. Two ATP-dependent Ca 2+ transport activities could be resolved on the basis of sensitivity to nitrate and affinity for Ca 2+. A low affinity Ca 2+ uptake system ( Km > 200 micromolar) was inhibited by nitrate and ionophores and is thought to represent a tonoplast localized H +/Ca 2+ antiport. A high affinity Ca 2+ uptake system ( Km = 6 micromolar) was not inhibited by nitrate, had reduced sensitivity to ionophores, and appeared to be associated with a population of low density endoplasmic reticulum vesicles that contaminated the tonoplast-enriched membrane fraction. Arrhenius plots of the temperature dependence of Ca 2+ transport in tomato membrane vesicles showed a sharp increase in activation energy at temperatures below 10 to 12°C that was not observed in red beet membrane vesicles. This low temperature effect on tonoplast Ca 2+/H + antiport activity could only by partially ascribed to an effect of low temperature on H +-ATPase activity, ATP-dependent H + transport, passive H + fluxes, or passive Ca 2+ fluxes. These results suggest that low temperature directly affects Ca 2+/H + exchange across the tomato fruit tonoplast, resulting in an apparent change in activation energy for the transport reaction. This could result from a direct effect of temperature on the Ca 2+/H + exchange protein or by an indirect effect of temperature on lipid interactions with the Ca 2+/H + exchange protein. 相似文献
20.
Washing corn ( Zea mays L.) root tissue in water causes loss of about one-third of the exchangeable Ca 2+ over the first 10 to 15 minutes. Upon transfer to K +-containing solutions, the tissue shows a short period of rapid K + influx which subsequently declines. Addition of 0.1 millimolar Ca 2+ decreases the initial rapid K + influx, but increases the sustained rate of K + and Cl − uptake. It was confirmed (Elzam and Hodges 1967 Plant Physiol 42: 1483-1488) that 0.1 millimolar Ca 2+ is more effective than higher concentrations for the initial inhibition, and that Mg 2+ will substitute. The inhibition arises from a mild shock affect of restoring Ca2+. With 0.1 millimolar Ca2+ net H+ efflux is blocked for 10 to 15 minutes and the cells are depolarized by about 30 millivolts. However, 1 millimolar Ca2+ rapidly produces increased K+ influx and blocks net H+ efflux for only a few minutes; blockage is preceded by a brief net H+ influx which may restore and increase ion transport by reactivating the plasmalemma H+-ATPase. Stimulation of electrogenic H+-pumping with fusicoccin eliminates the shock responses and minimizes Ca2+ effects on K+ influx. Fusicoccin also strongly decreases Ca2+ influx, but has no effect on Ca2+ efflux. Ice temperatures and high pH decreased Ca2+ efflux, but uncoupler and chlorpromazine did not. It is suggested that the inhibitory and promotive actions of Ca2+ are manifested through decreases or increases in the protonmotive force. 相似文献
|