scholarly journals Association of Phosphatidylinositol-Specific Phospholipase C with Calcium-Induced Biomineralization in the Coccolithophore Emiliania huxleyi

2020 ◽  
Vol 8 (9) ◽  
pp. 1389
Author(s):  
Onyou Nam ◽  
Iwane Suzuki ◽  
Yoshihiro Shiraiwa ◽  
EonSeon Jin
Keyword(s):  
Phospholipase C ◽  
Calcium Concentration ◽  
Biogeochemical Cycles ◽  
Emiliania Huxleyi ◽  
Ambient Seawater ◽  
Biomineralization Process ◽  
Cellular Events ◽  
Calcium Bicarbonate ◽  
Calcium Supply ◽  
Calcification Process

Biomineralization by calcifying microalgae is a precisely controlled intracellular calcification process that produces delicate calcite scales (or coccoliths) in the coccolithophore Emiliania huxleyi (Haptophycea). Despite its importance in biogeochemical cycles and the marine environment globally, the underlying molecular mechanism of intracellular coccolith formation, which requires calcium, bicarbonate, and coccolith-polysaccharides, remains unclear. In E. huxleyi CCMP 371, we demonstrated that reducing the calcium concentration from 10 (ambient seawater) to 0.1 mM strongly restricted coccolith production, which was then recovered by adding 10 mM calcium, irrespective of inorganic phosphate conditions, indicating that coccolith production could be finely controlled by the calcium supply. Using this strain, we investigated the expression of differentially expressed genes (DEGs) to observe the cellular events induced by changes in calcium concentrations. Intriguingly, DEG analysis revealed that the phosphatidylinositol-specific phospholipase C (PI-PLC) gene was upregulated and coccolith production by cells was blocked by the PI-PLC inhibitor U73122 under conditions closely associated with calcium-induced calcification. These findings imply that PI-PLC plays an important role in the biomineralization process of the coccolithophore E. huxleyi.

scholarly journals How far does phospholipase C activity depend on the cell calcium concentration? A study in intact cells

1987 ◽  
Vol 243 (2) ◽  
pp. 391-398 ◽  
Author(s):  
D Renard ◽  
J Poggioli ◽  
B Berthon ◽  
M Claret
Keyword(s):  
Phospholipase C ◽  
Calcium Concentration ◽  
Liver Cells ◽  
Resting Cells ◽  
High Concentration ◽  
Intact Cells ◽  
Phosphatidylinositol Phosphate ◽  
Isolated Liver Cells ◽  
193 Nm ◽  
Isolated Liver

The dependence of phospholipase C activity on the cytosolic Ca2+ concentration ([Ca2+]i) was studied in intact liver cells treated with the Ca2+-mobilizing hormone vasopressin, or not so treated. Phospholipase C (PLC) activity was estimated from the formation of [3H]inositol trisphosphate (InsP3) and the degradation of [3H]phosphatidylinositol 4,5-bisphosphate (PtdInsP2). The [Ca2+]i of the cells was clamped from 29 to 1130 nM by quin2 loading. This wide concentration range was obtained by loading the hepatocytes with a high concentration of the Ca2+ indicator in low-Ca2+ medium or by using the Ca2+ ionophore ionomycin in medium containing Ca2+. In resting cells, in which [Ca2+]i was 193 nM, treatment with 0.1 microM-vasopressin which stimulates liver PLC maximally, tripled InsP3 content and raised [Ca2+]i to 2 microM within 15 s. Lowering [Ca2+]i partially decreased cell InsP3 content as well as the ability of vasopressin to stimulate InsP3 formation maximally. At 29 nM, the lowest Ca2+ concentration obtained in isolated liver cells, basal InsP3 content was 64% of that measured in control cells. Addition of vasopressin no longer affected [Ca2+]i, but significantly increased InsP3 by 200%, although less than in the controls (300%). The maintenance of the greater part of the PLC response at constant [Ca2+]i indicated that, in the liver, InsP3 formation does not result from an increase in [Ca2+]i. The effects of lowering [Ca2+]i were reversible. When low cell [Ca2+]i was restored to a normal value, resting InsP3 content and the ability of vasopressin to stimulate InsP3 formation maximally by 300% were also restored. Raising [Ca2+]i from 193 to 1130 nM had little effect on the InsP3 content or the vasopressin-mediated increase in InsP3. In agreement with the stimulation of PLC activity by vasopressin, cell [3H]PtdInsP2 and total PtdInsP2 were degraded by application of this hormone for 15 s. In contrast, when [Ca2+]i was lowered to 29 nM, basal [3H]PtdInsP2 and total PtdInsP2 were increased by about 30%, [3H]PtdInsP2 was further increased by vasopressin, but total PtdInsP2 was not changed. These results show that, in intact hepatocytes, PLC is little affected by [Ca2+]i concentrations above 193 nM, but is partially dependent on Ca2+ below that value. They suggest that, in addition to activating PLC activity, vasopressin might stimulate PtdInsP2 synthesis, presumably via phosphatidylinositol-phosphate kinase, and that this pathway might predominate in cells with low [Ca2+]i.

Calcium requirements of plants

1969 ◽  
Vol 20 (3) ◽  
pp. 465 ◽  
Author(s):  
JF Loneragan ◽  
K Snowball
Keyword(s):  
Calcium Concentration ◽  
Dry Weight ◽  
Calcium Deficiency ◽  
Critical Values ◽  
Functional Requirement ◽  
Functional Requirements ◽  
Constant Concentration ◽  
Excess Calcium ◽  
Wide Range ◽  
Calcium Supply

Calcium concentrations in the tops and roots of 30 grasses, cereals, legumes, and herbs were examined for plants grown over a wide range of calcium concentrations (0.3 to 1000 µM) which were maintained constant in flowing culture solutions of pH 5.7. When plants were grown continuously in solutions of constant concentration, the relation between the calcium concentration in tops and the yield generally showed two regions. Increasing solution calcium concentrations from 0.3 to 2.5 µM increased the yield greatly, while calcium concentrations in the tops remained constant. By contrast, increasing solution concentrations from 10 to 1000 µM markedly increased concentrations in tops but in most species had relatively small effects on yield. At luxury calcium supply the concentrations in herb and legume tops were very much higher than those of grasses and cereals and were surprisingly similar to those of the same species grown in soil in the field. That calcium concentration in plant tops which remained constant while yield increased substantially is believed to indicate the minimal functional requirement of the tops for calcium. The average functional requirements of herb and legume tops (0.1–0.2% dry weight) were generally much lower than previously reported but were about twice those of grasses and cereals (0.05–0.1%). With the exception of Lupinus spp., no legume or herb had functional calcium requirements as low as those of any grass or cereal. When plants were transferred from 1000 to 0.3 µM calcium concentrations, they developed calcium deficiency symptoms and grew less than plants which had one-third to one-tenth the calcium concentrations in their tops but which had been grown continuously in solutions of low and constant concentration (2.5–10 µM). Excess calcium accumulated in the old leaves during luxury calcium supply but was not mobilized when plants were transferred to calcium-deficient solutions. It is suggested that variation in the conditions of calcium supply under which calcium deficiency develops partly accounts for the wide range of critical values used by various workers to diagnose deficiency in plants.

scholarly journals Endothelium-derived relaxing factor inhibits thrombin-induced platelet aggregation by inhibiting platelet phospholipase C

Blood ◽  
1992 ◽  
Vol 79 (1) ◽  
pp. 110-116
Author(s):  
W Durante ◽  
MH Kroll ◽  
PM Vanhoutte ◽  
AI Schafer
Keyword(s):  
Platelet Aggregation ◽  
Phospholipase C ◽  
Calcium Concentration ◽  
Umbilical Vein ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Relaxing Factor ◽  
Kinase C ◽  
Endothelium Derived Relaxing Factor ◽  
Induced Aggregation

Endothelium-derived relaxing factor (EDRF) inhibits platelet function, but the mechanism underlying this inhibitory effect is not known. To examine this, cultured acetylsalicylic acid (ASA)-treated endothelial cells (EC) from bovine aorta (BAEC) or from human umbilical vein (HUVEC) were incubated with washed, ASA-treated human platelets. Incubation of platelets with either BAEC or HUVEC resulted in inhibition of thrombin-induced platelet aggregation that was dependent on the number of EC added. This effect was potentiated by superoxide dismutase and reversed by treating EC with NG-nitro-L-arginine or by treating platelets with methylene blue, indicating that the inhibition of platelet aggregation was due to the release of EDRF by EC. EC significantly blocked the thrombin stimulated breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the production of phosphatidic acid in [32P]orthophosphate-labeled platelets and of inositol trisphosphate in [3H]myoinositol-labeled platelets. In addition, the thrombin-mediated activation of protein kinase C (PKC) and phosphorylation of myosin light chain were inhibited in the presence of EC. Finally, thrombin stimulated an increase in cytosolic ionized calcium concentration ([Ca2+]i) in fura2-loaded platelets that was abolished by concentrations of EC which also blocked thrombin- induced aggregation. These data indicate that EDRF blocks thrombin- induced platelet aggregation by inhibiting the activation of PIP2- specific phospholipase C and thereby suppressing the consequent activation of PKC and the mobilization of [Ca2+]i.

scholarly journals A molecular calcium integrator reveals a striatal cell-type driving aversion

2020 ◽  
Author(s):  
Christina K. Kim ◽  
Mateo I. Sanchez ◽  
Paul Hoerbelt ◽  
Lief E. Fenno ◽  
Robert C. Malenka ◽  
...  
Keyword(s):  
Nucleus Accumbens ◽  
Large Scale ◽  
Calcium Concentration ◽  
Modular Design ◽  
Cell Type ◽  
Neural Ensembles ◽  
Cellular Events ◽  
Large Scale Analysis ◽  
Genetic Tagging ◽  
A Cell

SUMMARYThe ability to record transient cellular events in the DNA or RNA of cells would enable precise, large-scale analysis, selection, and reprogramming of heterogeneous cell populations. Here we report a molecular technology for stable genetic tagging of cells that exhibit activity-related increases in intracellular calcium concentration (FLiCRE). We used FLiCRE to transcriptionally label activated neural ensembles in the nucleus accumbens of the mouse brain during brief stimulation of aversive inputs. Using single-cell RNA sequencing, we detected FLiCRE transcripts among the endogenous transcriptome, providing simultaneous readout of both cell-type and calcium activation history. We identified a cell-type in the nucleus accumbens activated downstream of long-range excitatory projections. Taking advantage of FLiCRE’s modular design, we expressed an optogenetic channel selectively in this cell-type, and showed that direct recruitment of this otherwise genetically-inaccessible population elicits behavioral aversion. The specificity and minute-resolution of FLiCRE enables molecularly-informed characterization, manipulation, and reprogramming of activated cellular ensembles.

scholarly journals Isozymes delta of phosphoinositide-specific phospholipase C.

1999 ◽  
Vol 46 (1) ◽  
pp. 91-98 ◽  
Author(s):  
T Pawełczyk
Keyword(s):  
Phospholipase C ◽  
Calcium Concentration ◽  
Intracellular Localization ◽  
Membrane Lipid ◽  
Kinase C ◽  
Pathological Conditions ◽  
Intracellular Signals ◽  
Starting Point ◽  
Regulation Of Activity ◽  
Regulate Protein

Phospholipase C (PLC, EC 3.1.4.11) is the major starting point in the phosphatidylinositol pathway, which generates intracellular signals that regulate protein kinase C and intracellular calcium concentration. To date, three major types of phosphoinositide-specific PLC species named beta, gamma and delta, have been characterized. This article reviews recent studies on isozymes delta of PLC. Four such isozymes have been cloned and termed delta1-4. Their structural organization, regulation of activity and the interaction with membrane lipid are considered. The intracellular localization of delta isozymes and distribution in various tissues are presented. Attention is given to the pathological conditions in which an abnormal protein level of PLC delta or its activity have been observed.

scholarly journals An Emiliania huxleyi pan-transcriptome reveals basal strain specificity in gene expression patterns

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ester Feldmesser ◽  
Shifra Ben-Dor ◽  
Assaf Vardi
Keyword(s):  
Gene Expression ◽  
Viral Infection ◽  
Expression Patterns ◽  
Protein Translation ◽  
Biogeochemical Cycles ◽  
Emiliania Huxleyi ◽  
Strain Specificity ◽  
Bloom Formation ◽  
Resistant Strains ◽  
Ecological Importance

AbstractEmiliania huxleyi is a cosmopolitan coccolithophore widespread in temperate oceans. This unicellular photoautotroph forms massive recurring blooms that play an important role in large biogeochemical cycles of carbon and sulfur, which play a role in climate change. The mechanism of bloom formation and demise, controlled by giant viruses that routinely infect these blooms, is poorly understood. We generated a pan-transcriptome of E. huxleyi, derived from three strains with different susceptibility to viral infection. Expression profiling of E. huxleyi sensitive and resistant strains showed major basal differences, including many genes that are induced upon viral infection. This suggests that basal gene expression can affect the host metabolic state and the susceptibility of E. huxleyi to viruses. Due to its ecological importance, the pan-transcriptome and its protein translation, applicable to many E. huxleyi strains, is a powerful resource for investigation of eukaryotic microbial communities.

scholarly journals Endothelium-derived relaxing factor inhibits thrombin-induced platelet aggregation by inhibiting platelet phospholipase C

Blood ◽  
1992 ◽  
Vol 79 (1) ◽  
pp. 110-116 ◽  
Author(s):  
W Durante ◽  
MH Kroll ◽  
PM Vanhoutte ◽  
AI Schafer
Keyword(s):  
Platelet Aggregation ◽  
Phospholipase C ◽  
Calcium Concentration ◽  
Umbilical Vein ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Relaxing Factor ◽  
Kinase C ◽  
Endothelium Derived Relaxing Factor ◽  
Induced Aggregation

Abstract Endothelium-derived relaxing factor (EDRF) inhibits platelet function, but the mechanism underlying this inhibitory effect is not known. To examine this, cultured acetylsalicylic acid (ASA)-treated endothelial cells (EC) from bovine aorta (BAEC) or from human umbilical vein (HUVEC) were incubated with washed, ASA-treated human platelets. Incubation of platelets with either BAEC or HUVEC resulted in inhibition of thrombin-induced platelet aggregation that was dependent on the number of EC added. This effect was potentiated by superoxide dismutase and reversed by treating EC with NG-nitro-L-arginine or by treating platelets with methylene blue, indicating that the inhibition of platelet aggregation was due to the release of EDRF by EC. EC significantly blocked the thrombin stimulated breakdown of phosphatidylinositol-4,5-bisphosphate (PIP2) and the production of phosphatidic acid in [32P]orthophosphate-labeled platelets and of inositol trisphosphate in [3H]myoinositol-labeled platelets. In addition, the thrombin-mediated activation of protein kinase C (PKC) and phosphorylation of myosin light chain were inhibited in the presence of EC. Finally, thrombin stimulated an increase in cytosolic ionized calcium concentration ([Ca2+]i) in fura2-loaded platelets that was abolished by concentrations of EC which also blocked thrombin- induced aggregation. These data indicate that EDRF blocks thrombin- induced platelet aggregation by inhibiting the activation of PIP2- specific phospholipase C and thereby suppressing the consequent activation of PKC and the mobilization of [Ca2+]i.

Studies on soil reaction: VI. The interaction of acid soils, calcium carbonate and water, in relation to the determination of “lime requirements.”

1925 ◽  
Vol 15 (2) ◽  
pp. 237-255 ◽  
Author(s):  
Edward M. Crowther ◽  
Wallace S. Martin
Keyword(s):  
Calcium Concentration ◽  
Empirical Relationship ◽  
Acid Soils ◽  
Soil Reaction ◽  
Titration Curves ◽  
Calcium Bicarbonate ◽  
Electrometric Titration ◽  
Single Determination ◽  
Bicarbonate Solutions

The variations in Hutchinson-MacLennan “lime requirement” with the amount of soil and calcium bicarbonate solution are shown to be connected with the buffer action of the soil. Indirect titration curves can be derived from the calcium bicarbonate results, and show a systematic divergence from the direct electrometric titration curves, owing to the variable calcium concentration of the final bicarbonate solutions. In the presence of calcium chloride both methods show lower pH values for a given base absorption and yield almost identical titration curves. The Hutchinson-MacLennan “lime requirement” is always less than the equivalent of the amount of calcium hydroxide necessary to give a neutral suspension in the electrometric titrations. The calcium bicarbonate solutions at equilibrium are always more acid than pH 6·2, but the “salt effect” tends to give results corresponding to a somewhat higher degree of neutralisation. “Lime requirements” should be obtained by interpolation to some arbitrary concentration, and an empirical relationship is given by which the interpolation may be made from a single determination. The Hutchinson-MacLennan method can give no indication of the intensity of soil acidity, but serves to estimate the amount of lime necessary to give a considerable reduction of acidity.

scholarly journals Somatostatin-induced paradoxical increase in intracellular Ca2+ concentration and insulin release in the presence of arginine vasopressin in clonal HIT-T15 β-cells

2002 ◽  
Vol 364 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Henrique CHENG ◽  
Sirintorn YIBCHOK-ANUN ◽  
Seung-Chun PARK ◽  
Walter H. HSU
Keyword(s):  
Phospholipase C ◽  
Insulin Release ◽  
Arginine Vasopressin ◽  
Receptor Agonist ◽  
Calcium Concentration ◽  
Somatostatin Receptors ◽  
Rapid Decline ◽  
Atpase Inhibitor ◽  
Β Cells ◽  
Induced Changes

Somatostatin, a hormone that signals via Gi/Go, usually inhibits increases in intracellular calcium concentration ([Ca2+]i) and insulin release from β-cells. We have found that in the presence of arginine vasopressin (AVP), which signals via Gq, somatostatin increased [Ca2+]i, leading to insulin release in HIT-T15 cells. The increase in [Ca2+]i by somatostatin was observed even after 60min of AVP treatment. Somatostatin alone failed to increase [Ca2+]i and insulin release. Somatostatin induced changes in [Ca2+]i in a biphasic pattern, characterized by a sharp and transient increase followed by a rapid decline to sub-basal levels. Pretreatment with pertussis toxin, which inactivates Gi/Go, abolished the effects of somatostatin. U-73122, an inhibitor of phospholipase C, antagonized the somatostatin-induced increase in [Ca2+]i. In Ca2+-free medium, somatostatin still increased [Ca2+]i. Depletion of intracellular Ca2+ stores with thapsigargin, a microsomal Ca2+-ATPase inhibitor, abolished somatostatin's effect. In the presence of bradykinin, another Gq-coupled receptor agonist, somatostatin also increased [Ca2+]i, but not in the presence of isoproterenol (a Gs-coupled receptor agonist) or medetomidine (a Gi/Go-coupled receptor agonist). Our findings suggest that somatostatin signals through Gi/Go, and involves phospholipase C and Ca2+ release from the endoplasmic reticulum. The increase in [Ca2+]i by somatostatin leads to insulin release. This cross-talk is specific to Gq and Gi/Go, and is not limited to the AVP and somatostatin receptors.

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