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1.
A study of calcium ion regulation in Anabaena 7120 and its derivative mutant (CSE2) strain impaired in ntcA gene were investigated in terms of altered morphological and physiological responses against various levels of calcium stress (0–100 mM). Calcium concentration of 10 mM was found to be inhibitory while 100 mM proved lethal for both wild type and mutant strain. The involvement of Ca 2+ in the regulation of cellular processes has been described in terms of an influx or efflux of Ca 2+ from the cytosol. A biphasic calcium uptake with difference in calcium influx and efflux rate was responsible for differential amount of remaining calcium which followed a decreasing trend both for wild type and mutant. Low K s 0.5 and high V max in mutant suggest heavy and less restricted influx of calcium ion. Further, the interactive effect of calcium influx/efflux rate, remaining Ca 2+ and intracellular levels of Na + and K + may be attributed for the degree of membrane damage and growth sustenance during exogenous supply of calcium salt. Widening in heterocyst spacing pattern, decreased heterocyst frequency and formation of abnormal cell structures at higher concentration (100 mM CaCl 2) suggest that calcium mediated regulatory process modulate heterocyst frequency and maintenance of cell structure. Further, poor regulation of calcium ion homeostasis in ntcA suggests that the calcium level and ntcA gene expression are inter-related. 相似文献
2.
Phosphoinositide (PI) and calcium metabolism were studied in guinea pig cerebral cortex synaptosomes. Mass amounts of inositol and inositol monophosphates, and the levels of free intrasynaptosomal calcium ([Ca 2+] i) were measured after KCl (60 mM), after a direct cholinergic agonist carbachol (CA, 1mM), and after their combination. Inositol, inositol-1-phosphate (Ins1P), inositol-4-phosphate (Ins4P) and [Ca 2+] i were measured with and without 10 mM LiCl in the incubation medium. CA-induced cholinergic stimulation elevated synaptosomal Ins4P levels by 40% but did not affect Ins1P or [Ca 2+] i. On the contrary, KCl elevated Ins1P by 50% and [Ca 2+] i by 40% above the resting level, and decreased inositol by 20%, whereas no alterations in Ins4P occurred. CA did not modify the response of KCl, but KCl abolished the elevation of Ins4P by CA. LiCl attenuated KCl-induced elevation of Ins1P but amplified the CA-induced elevation of Ins4P. The elevation of presynaptic [Ca 2+] i was accompanied by accumulation of Ins1P but not that of Ins4P. Hence, the present results suggest that presynaptic cholinergic stimulation and KCl-induced depolarization may activate different degradation pathways of inositolphosphate metabolism. 相似文献
3.
The influence of tetanus toxin in vitro on the release of exogenous [ 3H]GABA was studied with rat cerebral cortex slices. The influx, long-term accumulation and spontaneous efflux of GABA were not modified by the toxin. The release induced by high K + (50 mM) medium from the superfused slices pretreated with the toxin was significantly inhibited in a time- and dose-dependent fashion. This release was attenuated during superfusion with Ca 2+-free medium and the toxin no longer affected the remaining Ca 2+-independent release. The release induced by Na +-free media did not require extracellular Ca 2+ ions, and the toxin inhibited the release both with and without Ca 2+. The toxin treatment had no marked influence on the ouabain (20 μM) or veratrine (25–50 μM)-induced release of GABA. The toxin treatment in vitro appears to modify some step(s) in the stimulated release of GABA without affecting its unstimulated membrane transport. Tetanus toxin may thus prove a valuable tool in studying the mechanisms of the release of GABA and possibly other inhibitory transmitters in synapses of the central nervous system. 相似文献
4.
A self-referencing and non-invasive Ca 2+-sensitive vibrating electrode was used to assess the effects of hydrogen peroxide-induced oxidative challenges on the efflux and influx of calcium across the plasma membrane of single nerve cells cultured from abdominal ganglion of Aplysia californica. A reduced net efflux of Ca 2+ from the cell soma occurred immediately after the addition of hydrogen peroxide (0.0025 mM, 0.005 mM or 0.01 mM) to the culture medium, indicating damage to the cell membrane or Ca 2+ transport mechanism. There then followed a marked efflux, the extent and duration of which was related to the concentration of hydrogen peroxide used and which may reflect compensatory activity by the Ca 2+ regulatory mechanisms in the plasmalemma. No morphological changes were observed in cells challenged with 0.0025 mM hydrogen peroxide and the enhanced rate of Ca 2+ efflux rapidly decreased to pre-exposure values. Sustained and enhanced Ca 2+ effluxes from those cells exposed to 0.005 mM or 0.01 mM hydrogen peroxide were also consistent with regulatory pumping of Ca 2+ out of the cell although contraction and blebbing of neurites and swelling of the soma may indicate that a proportion of the efflux arose from release of Ca 2+ from disrupted intracellular stores. The vibrating electrode is a useful additional technique for the study of the pathogenesis of neurological conditions, as ionic fluxes across single nerve cells exposed to physiologically-relevant concentrations of free radicals can be monitored non-invasively for prolonged periods. 相似文献
5.
The effects of monovalent cations, inhibitors of metabolism dinitrophenol (DNP), carbonyl cyanide- p-trifluoromethoxyphenylhydrazone (FCCP), and KCN and temperature variations upon Ca 2+ fluxes in intact roots of barley ( Hordeum vulgare L. cv. Fergus and Herta) seedlings were investigated. 45Ca 2+ influx was depressed in CaSO 4-grown (low-salt) plants by the presence of NH 4+, K +, or Na + in the uptake medium. In contrast Ca 2+ influx was slightly increased by Li +. In low-salt roots pretreated with KCN and in roots preloaded with K + (high-K + plants), the presence of K + in the medium had no significant effect on Ca 2+ influx, while in roots preloaded with Na +, the presence of K + in the medium depressed Ca 2+ influx. In absolute terms, Ca 2+ influx was significantly greater in high-salt (both K + or Na + preloaded) than in low-salt roots.Patterns of 45Ca 2+ efflux in the absence and in the presence of K +, NH 4+, or Li + in the external medium showed that these monovalent cations caused stimulation of 45Ca 2+ efflux both from the cytoplasmic and vacuolar phases.It was noted that these modifications of Ca 2+ fluxes by monovalent cations are transient and characteristic of a transitional stage of cation uptake by low-salt roots. We conclude that, together with stimulated active H + efflux (another characteristic of this transitional stage), modifications of Ca 2+ fluxes during monovalent cation uptake by low-salt roots is a response directed towards the maintenance of electrical neutrality.Determination of net fluxes revealed that the plants were close to Ca 2+ flux equilibrium in the growth medium (0.5 mM CaSO 4). Transfer of these plants to 0.5 mM CaSO 4 + 0.25 mM K 2SO 4 caused a net release of CA 2+ into the external medium. 相似文献
6.
Ca 2+ transport by sarcoplasmic reticulum vesicles was examined by incubating sarcoplasmic reticulum vesicles (0.15 mg/ml) at 37°C in, either normal medium that contained 0.15 M sucrose, 0.1 M KCl, 60 μM CaCl 2, 2.5 mM ATP and 30 mM Tes at pH 6.8, or a modified medium for elimination of ADP formed from ATP hydrolysis by including, in addition, 3.6 mM phosphocreatine and 33 U/ml of creatine phosphokinase. In normal medium, Ca 2+ uptake of sarcoplasmic reticulum vesicles reached a plateau of about 100 nmol/mg. In modified medium, after this phase of Ca 2+ uptake, a second phase of Ca 2+ accumulation was initiated and reached a plateau of about 300 nmol/mg. The second phase of Ca 2+ accumulation was accompanied by phosphate uptake and could be inhibited by ADP. Since, under these experimental conditions, there was no significant difference of the rates of ATP hydrolysis in normal medium and modified medium, extra Ca 2+ uptake in modified medium but not in normal medium could not be explained by different phosphate accumulation in the two media. Unidirectional Ca 2+ influx of sarcoplasmic reticulum near steady state of Ca 2+ uptake was measured by pulse labeling with 45Ca 2+. The Ca 2+ efflux rate was then determined by subtracting the net uptake from the influx rate. At the first plateau of Ca 2+ uptake in normal medium, Ca 2+ influx was balanced by Ca 2+ efflux with an exchange rate of 240 nmol/mg per min. This exchange rate was maintained relatively constant at the plateau phase. In modified medium, the Ca 2+ exchange rate at the first plateau of Ca 2+ uptake was about half of that in normal medium. When the second phase of Ca 2+ uptake was initiated, both the influx and efflux rates started to increase and reached a similar exchange rate as observed in normal medium. Also, during the second phase of Ca 2+ uptake, the difference between the influx and efflux rates continued to increase until the second plateau phase was approached. In conditions where the formation of ADP and inorganic phosphate was minimized by using a low concentration of sarcoplasmic (7.5 μg/ml) and/or using acetyl phosphate instead of ATP, the second phase of Ca 2+ uptake was also observed. These data suggest that the Ca 2+ load attained by sarcoplasmic reticulum vesicles during active transport is modulated by ADP accumulated from ATP hydrolysis. ADP probably exerts its effect by facilitating Ca 2+ efflux, which subsequently stimulates Ca 2+ exchange. 相似文献
7.
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
8.
Ca 2+ transport by sarcoplasmic reticulum vesicles was examined by incubating sarcoplasmic reticulum vesicles (0.15 mg/ml) at 37°C in, either normal medium that contained 0.15 M sucrose, 0.1 M KCl, 60 μM CaCl 2, 2.5 mM ATP and 30 mM Tes at pH 6.8, or a modified medium for elimination of ADP formed from ATP hydrolysis by including, in addition, 3.6 mM phosphocreatine and 33 U/ml of creatine phosphokinase. In normal medium, Ca 2+ uptake of sarcoplasmic reticulum vesicles reached a plateau of about 100 nmol/mg. In modified medium, after this phase of Ca 2+ uptake, a second phase of Ca 2+ accumulation was initiated and reached a plateau of about 300 nmol/mg. The second phase of Ca 2+ accumulation was accompanied by phosphate uptake and could be inhibited by ADP. Since, under these experimental conditions, there was no significant difference of the rates of ATP hydrolysis in normal medium and modified medium, extra Ca 2+ uptake in modified medium but not in normal medium could not be explained by different phosphate accumulation in the two media. Unidirectional Ca 2+ influx of sarcoplasmic reticulum near steady state of Ca 2+ uptake was measured by pulse labeling with 45Ca 2+. The Ca 2+ efflux rate was then determined by subtracting the net uptake from the influx rate. At the first plateau of Ca 2+ uptake in normal medium, Ca 2+ influx was balanced by Ca 2+ efflux with an exchange rate of 240 nmol/mg per min. This exchange rate was maintained relatively constant at the plateau phase. In modified medium, the Ca 2+ exchange rate at the first plateau of Ca 2+ uptake was about half of that in normal medium. When the second phase of Ca 2+ uptake was initiated, both the influx and efflux rates started to increase and reached a similar exchange rate as observed in normal medium. Also, during the second phase of Ca 2+ uptake, the difference between the influx and efflux rates continued to increase until the second plateau phase was approached. In conditions where the formation of ADP and inorganic phosphate was minimized by using a low concentration of sarcoplasmic (7.5 μg/ml) and/or using acetyl phosphate instead of ATP, the second phase of Ca 2+ uptake was also observed. These data suggest that the Ca 2+ load attained by sarcoplasmic reticulum vesicles during active transport is modulated by ADP accumulated from ATP hydrolysis. ADP probably exerts its effect by facilitating Ca 2+ efflux, which subsequently stimulates Ca 2+ exchange. 相似文献
9.
The role of trans-sarcolemma membrane electron efflux in the α-adrenergic control of Ca 2+ influx in perfused rat heart was examined. Electron efflux was measured by monitoring the rate of reduction of extracellular ferricyanide and compared with changes in contractility, as an indirect assessment of changes in cytoplasmic Ca 2+ concentration. Methoxamine and phenylephrine each increased the rate of ferricyanide reduction from 80 to approx. 114 nmol/min per g wet wt. of heart, with half-maximal activation occurring at 10 μM for each agonist. Activation of the rate of ferricyanide reduction by both 10 μM methoxamine and 10 μM phenylephrine was blocked by the α-adrenergic antagonist, phenoxybenzamine, but not by the β-antagonist, propranolol. Stimulation of the rate of ferricyanide reduction by the α-agonist coincided with the increase in contractility, each reaching maximum values at approx. 80 s. Removal of the α-agonists led to parallel decreases in contractility and the rate of reduction, each returning to pre-stimulation values in approx. 400 s. In addition, the relationship between Ca 2+ and ferricyanide reduction was examined. Perfusion of the heart with medium containing 6 mM CaCl 2 significantly increased contractility and the rate of ferricyanide reduction. Perfusion of the heart with low Ca 2+ diminished contractility, did not affect the rate of ferricyanide reduction, but amplified the stimulatory effect of methoxamine on this rate. The increase in ferricyanide reduction by α-adrenergic agonists resulted from a change in the apparent Vmax, indicative of an increase in electron efflux sites in the plasma membrane. It is concluded that α-adrenergic control of electron efflux closely parallels changes in contractility and therefore changes in the cytoplasmic concentration of Ca 2+. The data suggest that α-agonist-mediated changes in electron efflux may lead to Ca 2+ influx. 相似文献
10.
Ca 2+ efflux from sarcoplasmic reticulum vesicles was studied by measurements of net Ca 2+ uptake, 45Ca 2+ flux and hydrolysis of energy-rich phosphate. The maximal Ca 2+ uptake capacity (150–200 nmol/mg protein at pH 6.7, 10 mM MgCl 2 and μ=0.26) was independent of the nature and concentration of the energy-donating substrate (ATP or carbamyl phosphate) and of temperature (15–35°C), suggesting coupling between influx and efflux of Ca 2+. In the presence of high concentrations of ATP, this efflux of Ca 2+ was much higher than the passive Ca 2+ permeation, measured after ATP or Ca 2+ depletion of the reaction medium. Ca 2+ efflux was imperceptible at vesicle filling levels below 35–40 nmol Ca 2+/mg protein, and uncorrelated to the inhibition of the Ca 2+-ATPase by high intravesicular Ca 2+ concentrations. Analysis of the data indicated that Ca 2+ efflux under our conditions probably is associated with one of the Ca 2+-ATPase partial reactions occurring after dephosphorylation, rather than with a reversal of the Ca 2+ translocation step in the phosphorylated state of the enzyme. Furthermore, passive Ca 2+ permeation may be concurrently reduced during the enzymatically active state. It is proposed that both Ca 2+ efflux and passive Ca 2+ permeation (Ca 2+ outflow) proceed via the same channels which are closed (occluded) during part of the Ca 2+-ATPase reaction cycle. 相似文献
11.
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
12.
The channel of the glutamate N-methyl- d-aspartate receptor (NMDAR) transports Ca 2+ approximately four times more efficiently than that of Ca 2+-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors (AMPAR). To investigate the basis of this difference in these glutamate receptors (GluRs), we measured the ratio of Cs + efflux and Ca 2+ influx in recombinant NMDAR and Ca 2+-permeable AMPAR channels expressed in human embryonic kidney 293 (HEK 293) cells over a wide voltage range. At any one potential, this biionic flux ratio was measured by quantifying the total charge and the charge carried by Ca 2+ using whole-cell currents and fluorometric techniques (dye overload) with Cs + internally and Ca 2+ externally (1.8 or 10 mM) as the only permeant ions. In AMPAR channels, composed of either GluR-A(Q) or GluR-B(Q) subunits, the biionic flux ratio had a biionic flux-ratio exponent of 1, consistent with the prediction of the Goldman-Hodgkin-Katz current equation. In contrast, for NMDAR channels composed of NR1 and NR2A subunits, the biionic flux-ratio exponent was ∼2, indicating a deviation from Goldman-Hodgkin-Katz. Consistent with these results, in NMDAR channels under biionic conditions with high external Ca 2+ and Cs + as the reference ions, Ca 2+ permeability (P Ca/P Cs) was concentration dependent, being highest around physiological concentrations (1–1.8 mM; P Ca/P Cs ≈ 6.1) and reduced at both higher (110 mM; P Ca/P Cs ≈ 2.6) and lower (0.18 mM; P Ca/P Cs ≈ 2.2) concentrations. P Ca/P Cs in AMPAR channels was not concentration dependent, being around 1.65 in 0.3–110 mM Ca 2+. In AMPAR and NMDAR channels, the Q/R/N site is a critical determinant of Ca 2+ permeability. However, mutant AMPAR channels, which had an asparagine substituted at the Q/R site, also showed a biionic flux-ratio exponent of 1 and concentration-independent permeability ratios, indicating that the difference in Ca 2+ transport is not due to the amino acid residue located at the Q/R/N site. We suggest that the difference in Ca 2+ transport properties between the glutamate receptor subtypes reflects that the pore of NMDAR channels has multiple sites for Ca 2+, whereas that of AMPAR channels only a single site. 相似文献
14.
Stimulation of 86Rb + efflux from isolated parotid acinar cells by carbchol was biphasic. The phases of stimulated 86Rb + efflux were separated on the basis of their relative requirements for extracellular Ca 2+. If the isolated cells were incubated in Ca 2+ free buffer containing 1.0 mM ethylene glycol bis (β-aminoethyl ether) N, N 1 - tetra acetic acid (EGTA) for 30 min. before adding carbachol an initial phase of 86Rb + efflux was observed. A second phase of 86Rb + efflux was obtained upon addition of 2.0 mM Ca 2+. However when cells were incubated for 60 min. in Ca 2+ free buffer containing 1.0 mM EGTA the initial phase of release caused by carbachol was inhibited by 95 percent. If the EGTA was titrated with Ca 2+ to give 1.0 mM Ca 2+, following the 60 min. depletion regimen, the second phase was observed. Although 60 min. of Ca 2+-depletion in EGTA buffer was required for complete inhibition of the effect of carbachol on the initial phase of 86Rb + efflux, the response was fully restored within 4 min. after the readdition of Ca 2+. 相似文献
15.
The characteristics of Ca 2+ transport across the excitable membrane of Paramecium aurelia were studied by measuring 45Ca 2+ influx and efflux. The intracellular concentration of free Ca 2+ in resting P. aurelia was at least ten times less than the extracellular concentration. Ca 2+ influx was easily measurable at 0°C, but not at 23°C. The influx of 45Ca 2+ was stimulated by the same conditions which cause membrane depolarization and ciliary reversal. Addition of Na + and K + (which stimulate ciliary reversal) resulted in a 10-fold increase in the rate of Ca 2+ influx. An externally applied, pulsed, electric field (1–2 mA/cm 2 of electrode surface), caused the rate of Ca 2+ influx to increase 3–5 times, with the extent of stimulation dependent on the current density and the pulse width Ca 2+ influx had the characteristics of a passive transport system and was associated with the chemically or electrically triggered Ca 2+ “gating” mechanism, which has been studied electrophysiologically. In contrast, Ca 2+ efflux appeared to be catalyzed by an active transport system. With cells previously loaded at 0°C with 45Ca 2+, Ca 2+ efflux was rapid at 23°C, but did not occur at 0°C. This active Ca 2+ efflux mechanism is probably responsible for maintaining the low internal Ca 2+ levels in unstimulated cells. 相似文献
16.
The effect of external calcium and sodium ion concentrations on the calcium fluxes on the Pelvetia fastigiata De Toni egg was measured. Decreasing external [Ca 2+] greatly increased the permeability of the eggs to Ca 2+; at 1 mM external Ca 2+ this permeability was 60 times as great as it was at the normal [Ca 2+] of 10 mM. Lowering the external [Na +] also increased Ca 2+ influx; at 2 mM Na +, the Ca 2+ influx was 2–3 times as great as it was at the normal [Na +] if choline was used as a Na + substitute. Lithium was less effective as a Na + substitute in increasing Ca 2+ influx. The extra Ca 2+ influx in low [Na +] seemed to be dependent on internal [Na +]. The Ca 2+ efflux increased transiently and then declined in low Na + media. 相似文献
17.
This report utilizes an Ussing-type apparatus to quantitative the unidirectional fluxes of Ca 2+ across the periosteal and endosteal membranes of frontal bones derived from calvaria of 20-day chick embryos. The influx was found to be proportional to the concentration of Ca 2+ and equal to 0.31 μmoles/cm 2 per h at a concentration of ultrafiltrable Ca 2+ of 1.75 mM. There were observable differences in the influx measured from periosteal or endosteal sides. The influx was found to be inversely proportional to decreasing temperature and increasing viscosity. The influx increased to 150% of the control flux when the incubation medium contained iodoacetate at a concentration of 1 mM and increased to 200% of control flux when the endosteum or periosteum was removed. These characteristics support the view that the influx is a passive flow with the integrity of cellular layer a controlling factor. The endosteal efflux was greater by a factor of 2 when compared to the periosteal efflux at 37 °C. When the temperature was reduced to 6 °C the endosteal to periosteal efflux ratio decreased to 1.26 indicating a temperature-sensitive component in the endosteal efflux. 相似文献
18.
Tetrastigma hemsleyanum suspension cells were treated with four metal salts to screen suitable elicitors for the promotion of plant cell biomass and flavonoid production. The effects of calcium ions (Ca 2+) on induction were also studied. It was found that the most effective elicitors were 50 μM of the heavy metal ion copper (Cu 2+) and 100 μM of the rare earth element cerium (Ce 3+). The maximal biomass levels under respective treatments over a 16-d culture period increased by 1.3- and 1.6-fold, and the total flavonoid content was 1.8- and 1.6-fold greater than the control, respectively. Reducing the exogenous Ca 2+ concentration or adding Ca 2+ antagonists (1 mM ethylene glycol-bis(2-aminoethylether)- N, N, N′, N-tetraacetc acid (EGTA) or 1 mM verapamil) strengthened inductive effects of metal elicitors and enhanced flavonoid production. However, 0.5 μM of the calcium ionophore A23187 showed contrary results. The increase in exogenous Ca 2+ concentration in the presence of A23187 suppressed H 2O 2 bursts and peroxidase activity caused by metal elicitors. The results suggest that Ca 2+ plays an inhibitory role in the plant cell response to metal elicitors. This suppression could have been caused by Ca 2+ preventing the cells from absorbing metal ions and then easing the induction, or because the decrease of Ca 2+ concentration worked as an induction signal. Therefore, reducing the Ca 2+ concentration in culture medium, or adding Ca 2+ antagonists could be used to improve flavonoid production and cell growth in combination with induction by metal elicitors during in vitro culture of T. hemsleyanum suspension cells. 相似文献
19.
The adaptation to extreme concentrations of Ca 2+ and its consequence on the properties of the 45Ca 2+ transport were studied in submerged mycelia of Trichoderma viride. The adaptation to low [Ca 2+] o did not cause changes in kinetic parameters of the 45Ca 2+ influx but the adaptation to high [Ca 2+] o increased the KM(Ca2+). The Vmax of the 45Ca 2+ influx decreased with the age of (non-adapted) mycelia with concomitant decrease of the KM(Ca2+) these changes were prevented in mycelia adapted to high Ca 2+. High [Ca 2+] o decreased the stimulation by the uncoupler, 3, 3′, 4′, 5-tetrachloro salicylanilide (TCS) (30 μM), as compared to the control, whereas the Ca 2+ chelator, EGTA, stimulated it. In the aged mycelia, the stimulation by TCS of the 45Ca 2+ influx faded away, in parallel with the activity of the H +-ATPase. The 45Ca 2+ efflux from mycelia was affected by TCS in a similar way as the 45Ca 2+ influx. The results demonstrate the adaptive responses of transport processes participating in the mycelial Ca 2+ homeostasis and ageing are in agreement with a notion that both Ca 2+-influx and-efflux are coupled by the H +-homeostasis at the plasma membrane. 相似文献
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