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1.
The phosphatidylinositol-specific phospholipase C, presumably a Zn-metalloenzyme, catalyzes the hydrolysis of phosphatidylinositol-4,5-bisphosphate to inositol-1,4,5-trisphosphate (IP3) and s,n-1,2-diacylglycerol (DAG). The activity of phosphatidylinositol-specific phospholipase C was measured indirectly by determination of the metabolites IP3 and DAG in Zn deficiency. For this purpose 24 male Sprague-Dawley rats with an average live mass of 117 g were divided into 2 groups of 12 animals each. The Zn-deficient and the control group received a semisynthetic casein diet with a Zn content of 1.6 ppm and 115 ppm, respectively. In order to prevent the reduced feed intake that occurs in Zn deficiency and the associated energy and protein depletion from interfering with the experimental parameters, all animals were fed four times daily by gastric tube. This made it possible to supply all animals with adequate nutrients and to synchronize the feed intake exactly. After 12 d, the depleted rats were in a severe state of Zn deficiency, as demonstrated by the reduction of Zn in the serum and the femur by 74% and 43%, respectively, and the 28% lower serum activity of alkaline phosphatase. The radioimmunologically determined concentrations of IP3 were reduced by a significant 53% in the testes of the Zn-deficient rats (0.24 nmol IP3/g wet wt) compared to the control animals (0.51 nmol IP3/g wet wt), while the IP3 concentration in the brain was not affected by the alimentary Zn supply (1.7 and 1.6 nmol IP3/g wet wt, respectively). The DAG concentrations in the testes (474 vs 471 nmol DAG/g wet wt) and the brain (594 vs 640 nmol DAG/g wet wt), which were determined by radioenzymatic methods, showed no significant differences in relation to the alimentary Zn supply. The fact that the Zn concentration in the Zn-deficient rats was reduced only in the testes and not in the brain and that high concentrations of DAG may also result from other metabolic processes suggests that the phosphatidylinositol-specific phospholipase C in the mammalian organism is a Zn-metalloenzyme whose activity is reduced in alimentary Zn deficiency in tissues suffering Zn loss.  相似文献   

2.
The purpose of the present study was to investigate, in force-fed rats, whether alimentary zinc (Zn) deficiency affects the activity of the Zn-metalloenzyme protein kinase C (PKC). The in vivo activity of PKC was determined by measuring the subcellular distribution of the enzyme between the cytosolic and the particulate fraction in brain and muscle. For this purpose, 24 male Sprague-Dawley rats with an average live mass of 126 g were divided into 2 groups of 12 animals each. The Zn-deficient and the control rats received a semisynthetic casein diet with a Zn content of 1.2 and 24.1 ppm, respectively. All animals were fed four times daily by gastric tube in order to ensure that the depleted animals also received adequate nutrients and to synchronize the feed intake exactly. After 12 d, the depleted rats were in a state of severe Zn deficiency, as demonstrated by a 70% lower serum Zn concentration and a 66% reduction in the serum activity of alkaline phosphatase. Neither the cytosolic nor the particulate fraction of the thigh muscle showed any difference between the depleted and the control animals as regards PKC activity/g of muscle. The specific activity of PKC/mg of protein in the cytosolic fraction of the muscle was not affected by alimentary zinc deficiency, whereas the specific activity of PKC in the particulate fraction of the muscle was reduced by a significant 10% in Zn deficiency (150±12 vs 135±14 pmol P/min/mg protein). In the brain, neither the cytosolic nor the particulate fraction revealed any difference in PKC activity/g of fresh weight or in the specific activity/mg of protein between the control and the Zn-deficient rats.  相似文献   

3.
The metabolism of exogenously added d-myo-[1-3H]inositol 1,4,5-trisphosphate (IP3) has been examined in microsomal membrane and soluble fractions of carrot (Daucus carota L.) cells grown in suspension culture. When [3H]IP3 was added to a microsomal membrane fraction, [3H]IP2 was the primary metabolite consisting of approximately 83% of the total recovered [3H] by paper electrophoresis. [3H]IP was only 6% of the [3H] recovered, and 10% of the [3H]IP3 was not further metabolized. In contrast, when [3H]IP3 was added to the soluble fraction, approximately equal amounts of [3H]IP2 and [3H]IP were recovered. Ca2+ (100 micromolar) tended to enhance IP3 dephosphorylation but inhibited the IP2 dephosphorylation in the soluble fraction by about 20%. MoO42− (1 millimolar) inhibited the dephosphorylation of IP3 by the microsomal fraction and the dephosphorylation of IP2 by the soluble fraction. MoO42−, however, did not inhibit the dephosphorylation of IP3 by the soluble fraction. Li+ (10 and 50 millimolar) had no effect on IP3 metabolism in either the soluble or membrane fraction; however, Li+ (50 millimolar) inhibited IP2 dephosphorylation in the soluble fraction about 25%.  相似文献   

4.
Erenoglu  B.  Nikolic  M.  Römheld  V.  Cakmak  I. 《Plant and Soil》2002,241(2):251-257
Using two bread wheat (Triticum aestivum) and two durum wheat (Triticum durum) cultivars differing in zinc (Zn) efficiency, uptake and translocation of foliar-applied 65Zn were studied to characterize the role of Zn nutritional status of plants on the extent of phloem mobility of Zn and to determine the relationship between phloem mobility of Zn and Zn efficiency of the used wheat cultivars. Irrespective of leaf age and Zn nutritional status of plants, all cultivars showed similar Zn uptake rates with application of 65ZnSO4 to leaf strips in a short-term experiment. Also with supply of 65ZnSO4 by immersing the tip (3 cm) of the oldest leaf of intact plants, no differences in Zn uptake were observed among and within both wheat species. Further, Zn nutritional status did not affect total uptake of foliar applied Zn. However, Zn-deficient plants translocated more 65Zn from the treated leaf to the roots and remainder parts of shoots. In Zn-deficient plants about 40% of the total absorbed 65Zn was translocated from the treated leaf to the roots and remainder parts of shoots within 8 days while in Zn-sufficient plants the proportion of the translocated 65Zn of the total absorbed 65Zn was about 25%. Although differences in Zn efficiency existed between the cultivars did not affect the translocation and distribution of 65Zn between roots and shoots. Bread wheats compared to durum wheats, tended to accumulate more 65Zn in shoots and less 65Zn in roots, particularly under Zn-deficient conditions. The results indicate that differences in expression of Zn efficiency between and within durum and bread wheats are not related to translocation or distribution of foliar-applied 65Zn within plants. Differential compartementation of Zn at the cellular levels is discussed as a possible factor determining genotypic variation in Zn efficiency within wheat.  相似文献   

5.
How Ca2+ oscillations are generated and fine-tuned to yield versatile downstream responses remains to be elucidated. In hepatocytes, G protein-coupled receptor-linked Ca2+ oscillations report signal strength via frequency, whereas Ca2+ spike amplitude and wave velocity remain constant. IP3 uncaging also triggers oscillatory Ca2+ release, but, in contrast to hormones, Ca2+ spike amplitude, width, and wave velocity were dependent on [IP3] and were not perturbed by phospholipase C (PLC) inhibition. These data indicate that oscillations elicited by IP3 uncaging are driven by the biphasic regulation of the IP3 receptor by Ca2+, and, unlike hormone-dependent responses, do not require PLC. Removal of extracellular Ca2+ did not perturb Ca2+ oscillations elicited by IP3 uncaging, indicating that reloading of endoplasmic reticulum stores via plasma membrane Ca2+ influx does not entrain the signal. Activation and inhibition of PKC attenuated hormone-induced Ca2+ oscillations but had no effect on Ca2+ increases induced by uncaging IP3. Importantly, PKC activation and inhibition differentially affected Ca2+ spike frequencies and kinetics. PKC activation amplifies negative feedback loops at the level of G protein-coupled receptor PLC activity and/or IP3 metabolism to attenuate IP3 levels and suppress the generation of Ca2+ oscillations. Inhibition of PKC relieves negative feedback regulation of IP3 accumulation and, thereby, shifts Ca2+ oscillations toward sustained responses or dramatically prolonged spikes. PKC down-regulation attenuates phenylephrine-induced Ca2+ wave velocity, whereas responses to IP3 uncaging are enhanced. The ability to assess Ca2+ responses in the absence of PLC activity indicates that IP3 receptor modulation by PKC regulates Ca2+ release and wave velocity.  相似文献   

6.

Background

Many eukaryotes, including plants and fungi make spores that resist severe environmental stress. The micro-organism Dictyostelium contains a single phospholipase C gene (PLC); deletion of the gene has no effect on growth, cell movement and differentiation. In this report we show that PLC is essential to sense the environment of food-activated spores.

Results

Plc-null spores germinate at alkaline pH, reduced temperature or increased osmolarity, conditions at which the emerging amoebae can not grow. In contrast, food-activated wild-type spores return to dormancy till conditions in the environment allow growth. The analysis of inositol 1,4,5-trisphosphate (IP3) levels and the effect of added IP3 uncover an unexpected mechanism how PLC regulates spore germination: i) deletion of PLC induces the enhanced activity of an IP5 phosphatase leading to high IP3 levels in plc-null cells; ii) in wild-type spores unfavourable conditions inhibit PLC leading to a reduction of IP3 levels; addition of exogenous IP3 to wild-type spores induces germination at unfavourable conditions; iii) in plc-null spores IP3 levels remain high, also at unfavourable environmental conditions.

Conclusions

The results imply that environmental conditions regulate PLC activity and that IP3 induces spore germination; the uncontrolled germination of plc-null spores is not due to a lack of PLC activity but to the constitutive activation of an alternative IP3-forming pathway.  相似文献   

7.
Cyanide-induced neurotoxicity is associated with altered cellular Ca2+ homeostasis resulting in sustained elevation of cytosolic Ca2+. In order to characterize the effect of cyanide on intracellular signaling mechanisms, the interaction of KCN with the inositol 1,4,5-triphosphate Ca2+ signaling system was determined in the PC12 cell line. KCN in the concentration range of 1.0–100 μM produced a rapid rise in intracellular IP3 levels (peak level occurred within 60 sec); 10 μM KCN elevated intracellular levels of IP3 to 148% of control levels. This response was mediated by phospholipase C (PLC) since U73122, a specific PLC inhibitor, blocked the response. Removal of Ca2+ from the incubation medium and chelation of intracellular Ca2+ with BAPTA partially attenuate the cyanide-stimulated IP3 generation, showing that the response is partially Ca2+ dependent. Also, treatment of cells with nifedipine or LaCl3, Ca2+ channel blockers, partially blocked the generation of IP3. This study shows that cyanide in concentrations as low as 1 μM stimulates IP3 generation that may be mediated by receptor and nonreceptor IP3 production since they have differential dependence on Ca2+. It is proposed that this response is an early intracellular signaling action that can contribute to altered Ca2+ homeostasis characteristic of cyanide neurotoxicity. © 1997 John Wiley & Sons, Inc.  相似文献   

8.
Critical events in the life cycle of malaria parasites are controlled by calcium‐dependent signalling cascades, yet the molecular mechanisms of calcium release remain poorly understood. The synchronized development of Plasmodium berghei gametocytes relies on rapid calcium release from internal stores within 10 s of gametocytes being exposed to mosquito‐derived xanthurenic acid (XA). Here we addressed the function of phosphoinositide‐specific phospholipase C (PI‐PLC) for regulating gametocyte activation. XA triggered the hydrolysis of PIP2 and the production of the secondary messenger IP3 in gametocytes. Both processes were selectively blocked by a PI‐PLC inhibitor, which also reduced the early Ca2+ signal. However, microgametocyte differentiation into microgametes was blocked even when the inhibitor was added up to 5 min after activation, suggesting a requirement for PI‐PLC beyond the early mobilization of calcium. In contrast, inhibitors of calcium release through ryanodine receptor channels were active only during the first minute of gametocyte activation. Biochemical determination of PI‐PLC activity was confirmed using transgenic parasites expressing a fluorescent PIP2/IP3 probe that translocates from the parasite plasmalemma to the cytosol upon cell activation. Our study revealed a complex interdependency of Ca2+ and PI‐PLC activity, with PI‐PLC being essential throughout gamete formation, possibly explaining the irreversibility of this process.  相似文献   

9.
The metabolism of phosphatidylinositol-4,5-bisphosphate (PIP2) changed during the culture period of the thermoacidophilic red alga Galdieria sulphuraria. Seven days after inoculation, the amount of PIP2 in the cells was 910 ± 100 pmol g−1 fresh weight; by 12 d, PIP2 levels increased to 1200 ± 150 pmol g−1 fresh weight. In vitro assays indicated that phosphatidylinositol monophosphate (PIP) kinase specific activity increased from 75 to 230 pmol min−1 mg−1 protein between d 7 and 12. When G. sulphuraria cells were osmostimulated, transient increases of up to 4-fold could be observed in inositol-1,4,5-trisphosphate (IP3) levels within 90 s, regardless of the age of the cells. In d-12 cells, the increase in IP3 was preceded by a transient increase of up to 5-fold in specific PIP kinase activity, whereas no such increase was detected after osmostimulation of d-7 cells. The increase in PIP kinase activity before IP3 signaling in d-12 cells indicates that there is an additional pathway for regulation of phosphoinositide metabolism after stimulation other than an initial activation of phospholipase C. Also, the rapid activation of PIP2 biosynthesis in cells with already-high PIP2 levels suggests that the PIP2 present was not available for signal transduction. By comparing the response of the cells at d 7 and 12, we have identified two potentially distinct pools of PIP2.  相似文献   

10.
Inositol 1,4,5-trisphosphate receptors (IP3Rs) are intracellular Ca2+ channels that elevate cytoplasmic Ca2+ in response to the second messenger IP3. Here, we describe the identification and in vivo functional characterization of the planarian IP3R, the first intracellular Ca2+ channel to be defined in flatworms. A single IP3R gene in Dugesia japonica encoded a 2666 amino acid protein (Dj.IP3R) that shared well conserved structural features with vertebrate IP3R counterparts. Expression of an NH2-terminal Dj.IP3R region (amino acid residues 223–585) recovered high affinity 3H-IP3 binding (0.9 ± 0.1 nM) which was abolished by a single point mutation of an arginine residue (R495L) important for IP3 coordination. In situ hybridization revealed that Dj.IP3R mRNA was most strongly expressed in the pharynx and optical nerve system as well as the reproductive system in sexualized planarians. Consistent with this observed tissue distribution, in vivo RNAi of Dj.IP3R resulted in a decreased egg-laying behavior suggesting Dj.IP3R plays an upstream role in planarian reproductive physiology.  相似文献   

11.
Reactive oxygen species (ROS) stimulate cytoplasmic [Ca2+] ([Ca2+]c) signaling, but the exact role of the IP3 receptors (IP3R) in this process remains unclear. IP3Rs serve as a potential target of ROS produced by both ER and mitochondrial enzymes, which might locally expose IP3Rs at the ER-mitochondrial associations. Also, IP3Rs contain multiple reactive thiols, common molecular targets of ROS. Therefore, we have examined the effect of superoxide anion (O2) on IP3R-mediated Ca2+ signaling. In human HepG2, rat RBL-2H3, and chicken DT40 cells, we observed [Ca2+]c spikes and frequency-modulated oscillations evoked by a O2 donor, xanthine (X) + xanthine oxidase (XO), dose-dependently. The [Ca2+]c signal was mediated by ER Ca2+ mobilization. X+XO added to permeabilized cells promoted the [Ca2+]c rise evoked by submaximal doses of IP3, indicating that O2 directly sensitizes IP3R-mediated Ca2+ release. In response to X+XO, DT40 cells lacking two of three IP3R isoforms (DKO) expressing either type 1 (DKO1) or type 2 IP3Rs (DKO2) showed a [Ca2+]c signal, whereas DKO expressing type 3 IP3R (DKO3) did not. By contrast, IgM that stimulates IP3 formation, elicited a [Ca2+]c signal in every DKO. X+XO also facilitated the Ca2+ release evoked by submaximal IP3 in permeabilized DKO1 and DKO2 but was ineffective in DKO3 or in DT40 lacking every IP3R (TKO). However, X+XO could also facilitate the effect of suboptimal IP3 in TKO transfected with rat IP3R3. Although in silico studies failed to identify a thiol missing in the chicken IP3R3, an X+XO-induced redox change was documented only in the rat IP3R3. Thus, ROS seem to specifically sensitize IP3Rs through a thiol group(s) within the IP3R, which is probably inaccessible in the chicken IP3R3.  相似文献   

12.
Summary Maize and pea bean plants were grown for 2 weeks in Zn-deficient soil fertilized with varying levels of Fe and Zn. The plants were then exposed to C14O2 for 2 minutes and after harvest the ethanolsoluble photosynthate was fractionated into carbohydrates, organic acids, and amino acids. There appeared to be a general increase in the CO2 assimilation rate by maize with increasing rate of Zn; rates were slightly higher with applied Fe, at each Zn level. In contrast to maize, the rate of assimilation by pea beans was unaffected by substrate Zn and was slightly lower with application of Fe, especially in the carbohydrate fraction. Increasing rates of applied Zn had little effect on concentration of Fe and Mn in the maize or pea bean tops. However, application of Fe resulted in a depression in Zn concentration of maize. Despite the relatively high levels of Zn in the tissue of both species, there was no increase in total organic acids assimilated or any indication of gross metabolic imbalances.  相似文献   

13.
We previously reported the emerging role of CD137–CD137L interaction in inflammation and atherosclerosis. The mechanism of CD137–CD137L interaction may be related to a variety of signaling pathways. The most important signaling pathway involves the activation of phospholipase C(PLC) which induces the diacylglycerol–protein kinase C(DAG–PKC) and the inositol trisphosphate-intracellular free calcium (IP3-[Ca2+]i) pathway. In the current study, we investigated whether CD137–CD137L interaction can stimulate the PLC signaling pathway in human umbilical vein endothelial cells (HUVEC). The diacylglycerol (DAG) and inositol trisphosphate (IP3) levels in HUVEC were measured by radioenzymatic assay. The activity of protein kinase (PKC) was detected by its ability to transfer phosphate from [γ-32P]ATP to lysine-rich histone. The [Ca2+]i concentrations were measured by flow cytometric analysis. The DAG level and PKC activity were increased in a concentration-dependent, biphasic manner in HUVEC induced by anti-CD137. PKC activity was mainly in the cytosol at rest, and then translocated to the membrane when stimulated by anti-CD137. Similarly, rapid IP3 formation induced by anti-CD137 coincided with the peak of the DAG level. Moreover, anti-CD137 induced peak [Ca2+]i responses including the rapid transient phase and the sustained phase. However, anti-CD137L suppressed the activation of the DAG–PKC and IP3-[Ca2+]i signaling pathway, which was stimulated by anti-CD137 in HUVEC. In conclusion, the data suggested that CD137–CD137L interaction induces robust activation of the PLC signaling pathway in HUVEC.  相似文献   

14.
Background information. In endocrine cells, IP3R (inositol 1,4,5‐trisphosphate receptor), a ligand‐gated Ca2+ channel, plays an important role in the control of intracellular Ca2+ concentration. There are three subtypes of IP3R that are distributed differentially among cell types. RINm5F cells express almost exclusively the IP3R‐3 subtype. The purpose of the present study was to investigate the effect of PKA (protein kinase A) on the activity of IP3R‐3 in RINm5F cells. Results. We show that immunoprecipitated IP3R‐3 is a good substrate for PKA. Using a back‐phosphorylation approach, we show that endogenous PKA phosphorylates IP3R‐3 in intact RINm5F cells. [3H]IP3 (inositol 1,4,5‐trisphosphate) binding affinity and IP3‐induced Ca2+ release activity were enhanced in permeabilized cells that were pre‐treated with forskolin or PKA. The PKA‐induced enhancement of IP3R‐3 activity was also observed in intact RINm5F cells stimulated with carbachol and epidermal growth factor, two agonists that use different receptor types to activate phospholipase C. Conclusion. The results of the present study reveal a converging step where the cAMP and the Ca2+ signalling systems act co‐operatively in endocrine cell responses to external stimuli.  相似文献   

15.
Spinocerebellar ataxia type 15 (SCA15) is a group of human neurodegenerative disorders characterized by a slowly progressing pure cerebellar ataxia. The inositol 1,4,5-trisphosphate (IP3) receptor type 1 (IP3R1) is an intracellular IP3-induced Ca2+ release channel that was recently identified as a causative gene for SCA15. In most case studies, a heterozygous deletion of the IP3R1 gene was identified. However, one Japanese SCA15 family was found to have a Pro to Leu (P1059L) substitution in IP3R1. To investigate the effect of the P1059L mutation, we analyzed the channel properties of the mutant human IP3R1 by expressing it in an IP3R-deficient B lymphocyte cell line. The P1059L mutant was a functional Ca2+ release channel with a twofold higher IP3 binding affinity compared to wild-type IP3R1. The cooperative dependence of the Ca2+ release activity of the mutant on IP3 concentration was reduced, but both wild-type and mutant receptors produced similar B cell receptor-induced Ca2+ signals. These results demonstrate that the Ca2+ release properties of IP3R1 are largely unaffected by the P1059L mutation.  相似文献   

16.
Stimulation of A2A receptors (A2A R) coupled to Gs/olf protein activates Adenylyl cyclase (AC) leading to the release of cAMP which activates the cAMP-dependent PKA phosphorylation. The possible role of A2A R in the modulation of free cytosolic Ca2+ concentration ([Ca2+]i) involving IP3, cAMP and PKA was investigated in HEK 293-A2A R. The levels of IP3 and cAMP were observed by enzyme immunoassay detection method and [Ca2+]i using Fluo-4 AM. Moreover, cAMP-dependent PKA was determined using the PKA Colorimetric Activity Kit. We observed that the cells pre-treated with A2A R agonist NECA showed increased levels of cAMP, PKA, IP3 and [Ca2+]i levels. However, the reverse effect was observed with A2A R antagonists (ZM241385 and caffeine). Blocking the Gαq/PLC/DAG/IP3 pathway with neomycin, a PLC inhibitor did not affect the modulation of IP3 and [Ca2+]i levels in HEK 293-A2A R cells. To investigate the Gαi/AC/cAMP/PKA, HEK 293-A2A R cells pre-treated with pertussis toxin followed by forskolin in the presence of A2A R agonist (NECA) showed no effect on cAMP levels. Further, Gαs/AC/cAMP/PKA pathway was investigated to elucidate the role of cAMP-dependent PKA in IP3 mediated [Ca2+]i modulation. In the HEK 293-A2A R cells pre-treated with PKA inhibitor KT5720 and treated with NECA led to inhibit the IP3 and [Ca2+]i levels. The study distinctly demonstrated that A2A R modulates IP3 levels to release the [Ca2+]i via cAMP-dependent PKA. The role of A2A R mediated Gαs pathway inducing IP3 mediated [Ca2+]i release may open new avenues in the therapy of neurodegenerative disorder.  相似文献   

17.
There is substantial evidence that crosstalk between the proliferation and Ca2+-signaling pathways plays a critical role in the regulation of normal physiological functions as well as in the pathogenesis of a variety of abnormal processes. In non-excitable cells, intracellular Ca2+ is mobilized through inositol 1,4,5-trisphosphate sensitive Ca2+ channels (IP3R) expressed on the endoplasmic reticulum. Here we report that mTOR, a point of convergence for signals from mitogenic growth factors, nutrients and cellular energy levels, phosphorylates the IP3R-2, the predominant isoform of IP3R in AR4-2J cells. Pretreatment with the mTOR inhibitor rapamycin, decreased carbachol-induced Ca2+ release in AR4-2J cells. Rapamycin also decreased IP3-induced Ca2+ release in permeabilized AR4-2J cells. We also showed that IGF-1 potentiates carbachol-induced Ca2+ release in AR4-2J cells, an effect that was prevented by rapamycin. Rapamycin also decreased carbachol-induced Ca2+ release in HEK 293A cells in which IP3R-1 and IP3R-3 had been knocked down. These results suggest that mTOR potentiates the activity of IP3R-2 by a phosphorylation mechanism. This conclusion supports the concept of crosstalk between Ca2+ signaling and proliferation pathways and thus provides another way by which intracellular Ca2+ signals are finely encoded.  相似文献   

18.
Low-Zn seed (around 80 ng Zn per seed) and high-Zn seed (around 160 ng Zn per seed) of Zhongyou 821 (a traditional Brassica napus genotype from China found to be Zn-inefficient in our previous experiments), Narendra (Zn-efficient B. napus genotype from Australia) and CSIRO-1 (a Zn-efficient B. juncea genotype from Australia) oilseed rape genotypes were sown in pots containing Zn-deficient siliceous sand fertilized with low Zn supply (0.05 mg Zn kg–1 soil) or high Zn supply (2.0 mg Zn kg–1 soil) in a controlled environment. After six weeks, plants derived from the high-Zn seed had better seedling vigour, increased root and shoot growth, more leaf area and chlorophyll concentration in fresh leaf, and higher Zn uptake in shoot compared to those from low-Zn seed at low Zn supply; the impact of high-Zn seed was more marked in Zhongyou 821 compared with CSIRO-1 and Narendra. The influence of high-Zn seed was dissipated at high Zn supply. CSIRO-1 was superior in terms of shoot dry matter production and Zn uptake in shoots at low Zn supply. The results demonstrate that although oilseed rape has very small seeds (about 3 mg per seed weight) compared with wheat (30 mg per seed weight), Zn reserves present in this very small seed still have a strong impact on early vegetative growth as well as on Zn uptake of plants in Zn-deficient soils. The results suggest that sowing high-Zn seed coupled with growing Zn-efficient genotypes may help in sustaining the production of oilseed rape in Zn-deficient soils, and this has implications for improved seed technology.  相似文献   

19.
Calcium ions (Ca2+) released from inositol trisphosphate (IP3)-sensitive intracellular stores may participate in both the transient and extended regulation of neuronal excitability in neocortical and hippocampal pyramidal neurons. IP3 receptor (IP3R) antagonists represent an important tool for dissociating these consequences of IP3 generation and IP3R-dependent internal Ca2+ release from the effects of other, concurrently stimulated second messenger signaling cascades and Ca2+ sources. In this study, we have described the actions of the IP3R and store-operated Ca2+ channel antagonist, 2-aminoethoxydiphenyl-borate (2-APB), on internal Ca2+ release and plasma membrane excitability in neocortical and hippocampal pyramidal neurons. Specifically, we found that a dose of 2-APB (100 μM) sufficient for attenuating or blocking IP3-mediated internal Ca2+ release also raised pyramidal neuron excitability. The 2-APB-dependent increase in excitability reversed upon washout and was characterized by an increase in input resistance, a decrease in the delay to action potential onset, an increase in the width of action potentials, a decrease in the magnitude of afterhyperpolarizations (AHPs), and an increase in the magnitude of post-spike afterdepolarizations (ADPs). From these observations, we conclude that 2-APB potently and reversibly increases neuronal excitability, likely via the inhibition of voltage- and Ca2+-dependent potassium (K+) conductances.  相似文献   

20.
We investigated the direct effect of inositol 1,4,5-trisphosphate (IP3) and ryanodine receptor agonists on Ca2+ release from vesicles of a rat liver Golgi apparatus (GA) enriched fraction, which were actively loaded with 45Ca2+. Results in GA were compared with those obtained in a rat liver endoplasmic reticulum (ER) enriched fraction. The addition of IP3 at concentrations ranging from 100 nm to 100 μm, in the presence of thapsigargin, a specific inhibitor of sarcoplasmic/endoplasmic reticulum Ca2+-ATPases, promoted a rapid decrease in the Ca2+ content of GA vesicles. The amount of Ca2+ released from the vesicles was a function of IP3 concentration, reaching about 60% in both GA and ER fractions at 100 μm IP3. Calcium release was inhibited by heparin, an antagonist of IP3 receptors. Calcium exhibited a bell-shaped effect on IP3-dependent Ca2+ released from GA vesicles: it activated Ca2+ release at concentrations up to 1 μm, and inhibited it at higher concentrations. In contrast to that found in the endoplasmic reticulum fraction, none of the ryanodine receptor agonists tested (cyclic ADP-ribose, caffeine and ryanodine) significantly induced Ca2+ release from GA fraction vesicles in the presence of thapsigargin. Our results indicate the presence of an IP3-sensitive Ca2+ release mechanism in the Golgi apparatus membrane analogous to that of the ER. However, a Ca2+ release mechanism sensitive to ryanodine receptor agonists like that of ER is not evident in the GA membrane. Received: 13 March 2000/Revised: 13 July 2000  相似文献   

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