Nicotinamide alters the calcium release pattern and the degradation of MPF activity after fertilisation in ascidian oocytes

Zygote ◽  
1999 ◽  
Vol 7 (3) ◽  
pp. 255-260 ◽  
Author(s):  
Martin Wilding ◽  
Marcella Marino ◽  
Daniela Dale
Keyword(s):  
Cell Cycle ◽  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Embryo Development ◽  
Calcium Release ◽  
Calcium Signalling ◽  
Membrane Current ◽  
Calcium Induced Calcium Release ◽  
Nicotinamide Treatment ◽  
Meiosis I

Fertilisation in ascidian oocytes triggers a plasma membrane current, the release of intracellular calcium and the degradation of Maturation Promoting Factor (MPF) activity leading to the completion of meiosis and the initiation of embryo development. We have previously shown that the fertilisation current in ascidians is produced through the metabolism of nicotinamide nucleotide (NN) metabolites to ADP ribose. In this study we have used nicotinamide to test whether NN metabolism plays additional roles in fertilisation in ascidians. Nicotinamide treatment blocked calcium-induced calcium release (CICR) and arrested the cell cycle prior to the completion of meiosis I. Nicotinamide further prevented the abolition of MPF activity after fertilisation. Interestingly, nicotinamide treatment caused ascidian oocytes to form interphase-like pronuclei after fertilisation, despite the high MPF activity. The data demonstrate that NN metabolism is involved in calcium signalling through CICR and further suggest that a NN metabolite acts as a messenger connecting MPF activity to the formation of the meiotic apparatus.

scholarly journals Membrane junctions in xenopus eggs: their distribution suggests a role in calcium regulation

1983 ◽  
Vol 96 (4) ◽  
pp. 1159-1163 ◽  
Author(s):  
DM Gardiner ◽  
RD Grey
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Egg Activation ◽  
Electron Dense Material ◽  
Intracellular Calcium Release ◽  
Cortical Endoplasmic Reticulum ◽  
Center Distance ◽  
Lines Of Evidence

We have observed the presence of membrane junctions formed between the plasma membrane and cortical endoplasmic reticulum of mature, unactivated eggs of xenopus laevis. The parallel, paired membranes of the junction are separated by a 10-mn gap within which electron-dense material is present. This material occurs in patches with an average center-to-center distance of approximately 30 nm. These junctions are rare in immature (but fully grown) oocytes (approximately 2 percent of the plasma membrane is associated with junctions) and increase dramatically during progesterone-induced maturation. Junctions in the mature, unactivated egg are two to three times more abundant in the animal hemisphere (25-30 percent of the plasma membrane associated with junction) as compared with the vegetal hemisphere (10-15 percent). Junction density decreases rapidly to values characteristic of immature oocytes in response to egg activation. The plasma membrane-ER junctions of xenopus eggs are strikingly similar in structure to membrane junctions in muscle cells thought to be essential in the triggering of intracellular calcium release from the sarcoplasmic reticulum. In addition, the junctions' distinctive, animal-vegetal polarity of distribution, their dramatic appearance during maturation, and their disapperance during activation are correlated with previously documented patterns of calcium-mediated events in anuran eggs. We discuss several lines of evidence supporting the hypothesis that these junctions in xenopus eggs are sites that transduce extracellular events into intracellular calcium release during fertilization and activation of development.

Intracellular calcium stores are involved in growth hormone-releasing hormone signal transduction in rat somatotrophs

1999 ◽  
Vol 77 (7) ◽  
pp. 520-528 ◽  
Author(s):  
Audrey Petit ◽  
Catherine Bleicher ◽  
Benoît T Lussier
Keyword(s):  
Growth Hormone ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Calcium Stores ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Intracellular Ca ◽  
Calcium Induced Calcium Release

In rat pituitary somatotrophs, the stimulation of growth hormone secretion by growth hormone-releasing hormone (GHRH) is a Ca2+-dependent event involving Ca2+ influx. The presence of calcium-induced calcium release (CICR) Ca2+ stores has been suggested in these cells. The aim of our study was to demonstrate the presence of CICR stores in rat somatotrophs and to determine their function in GHRH Ca2+ signalling. To this end we measured cytosolic free Ca2+ concentration ([Ca2+]i), using indo-1 in purified rat somatotrophs in primary culture, while altering intracellular Ca2+ stores. Ionomycin (10 µM) or 4-bromo-A23187 (10 µM), used to mobilise organelle-bound Ca2+, raised [Ca2+]i in the absence of extracellular Ca2+. Caffeine (5 to 50 mM), used to mobilise Ca2+ from CICR stores, transiently raised [Ca2+]i in 65% of cells tested. The response to 40 mM caffeine was abolished when Ca2+ stores were depleted, with 1 µM thapsigargin or with 10 µM ryanodine. All cells that responded to 40 mM caffeine responded to 10 nM GHRH. The [Ca2+]i response to 10 nM GHRH was reversible and repeatable. However, the second response was 38% smaller than the first. Ryanodine treatment abolished the reduction in the second [Ca2+]i response, while thapsigargin increased the reduction by 67%. We conclude that rat somatotrophs possess CICR Ca2+ stores and that they account for 30-35% of the GHRH-induced increase in [Ca2+]i, and that their partial depletion is involved in somatotroph desensitization.Key words: somatotrophs, growth hormone-releasing hormone, intracellular calcium, calcium stores, calcium-induced calcium release.

Dehydroepiandrosterone inhibits intracellular calcium release in β-cells by a plasma membrane-dependent mechanism

Steroids ◽  
2006 ◽  
Vol 71 (8) ◽  
pp. 691-699 ◽  
Author(s):  
Dongmin Liu ◽  
Min Ren ◽  
Xinyu Bing ◽  
Corey Stotts ◽  
Sundeep Deorah ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Β Cells ◽  
Intracellular Calcium Release ◽  
Dependent Mechanism

scholarly journals The Builders of the Junction: Roles of Junctophilin1 and Junctophilin2 in the Assembly of the Sarcoplasmic Reticulum–Plasma Membrane Junctions in Striated Muscle

Biomolecules ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 109
Author(s):  
Stefano Perni
Keyword(s):  
Plasma Membrane ◽  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Cardiac Muscle ◽  
Structure Prediction ◽  
Calcium Release ◽  
Striated Muscle ◽  
Short Review ◽  
Published Data ◽  
Intracellular Calcium Release

Contraction of striated muscle is triggered by a massive release of calcium from the sarcoplasmic reticulum (SR) into the cytoplasm. This intracellular calcium release is initiated by membrane depolarization, which is sensed by voltage-gated calcium channels CaV1.1 (in skeletal muscle) and CaV1.2 (in cardiac muscle) in the plasma membrane (PM), which in turn activate the calcium-releasing channel ryanodine receptor (RyR) embedded in the SR membrane. This cross-communication between channels in the PM and in the SR happens at specialized regions, the SR-PM junctions, where these two compartments come in close proximity. Junctophilin1 and Junctophilin2 are responsible for the formation and stabilization of SR-PM junctions in striated muscle and actively participate in the recruitment of the two essential players in intracellular calcium release, CaV and RyR. This short review focuses on the roles of junctophilins1 and 2 in the formation and organization of SR-PM junctions in skeletal and cardiac muscle and on the functional consequences of the absence or malfunction of these proteins in striated muscle in light of recently published data and recent advancements in protein structure prediction.

Ectocellular in vitro and in vivo metabolism of cADP-ribose in cerebellum

1996 ◽  
Vol 320 (2) ◽  
pp. 665-671 ◽  
Author(s):  
Antonio DE FLORA ◽  
Lucrezia GUIDA ◽  
Luisa FRANCO ◽  
Elena ZOCCHI ◽  
Mario PESTARINO ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Granule Cells ◽  
Cerebellar Granule Cells ◽  
Adult Rat ◽  
Transmembrane Glycoprotein ◽  
Adp Ribosyl Cyclase ◽  
Calcium Induced Calcium Release

CD38, a type II transmembrane glycoprotein predominantly expressed in blood cells, is a bifunctional ectoenzyme directly involved in the metabolism of cADP-ribose (cADPR). This is a potent Ca2+ mobilizer in several types of cells. The relationship between the ectocellular site of cADPR production and its intracellular calcium-related functions is poorly understood. Cultured rat cerebellar granule cells showed both enzymic activities of CD38, ADP-ribosyl cyclase and cADPR hydrolase, at a ratio of 16 to 1 respectively, and were immunostained by the anti-(human CD38) monoclonal antibody IB4. In these cells externally added cADPR and β-NAD+ (the precursor of cADPR), but not α-NAD+ or ADP-ribose, enhanced the peak of the depolarization-induced rise in intracellular Ca2+ concentration. This effect was inhibited by 1 µM ryanodine, suggesting a potentiation of calcium-induced calcium release by cADPR. CD38 ectoenzyme activities, ADP-ribosyl cyclase and cADPR hydrolase, were also demonstrated in vivo by microdialysis of adult rat cerebellum, where IB4 bound to granule neurons selectively. Trace amounts (11.5±3.8 nM) of NAD+ were detected by microdialysis sampling and sensitive assays in the basal interstitial fluid of the cerebellum. These results provide a link between ectocellular cADPR turnover and intracellular calcium mobilization in cerebellum.

Soluble extracts from ascidian spermatozoa trigger intracellular calcium release independently of the activation of the ADP ribose channel

Zygote ◽  
1998 ◽  
Vol 6 (2) ◽  
pp. 149-154 ◽  
Author(s):  
Martin Wilding ◽  
Brian Dale
Keyword(s):  
Nitric Oxide ◽  
Plasma Membrane ◽  
Intracellular Calcium ◽  
Metabolic Pathway ◽  
Metabolic Pathways ◽  
Calcium Release ◽  
Ciona Intestinalis ◽  
Calcium Transient ◽  
Calcium Oscillations ◽  
Repetitive Pattern

We have injected soluble extracts of sperm from the ascidian Ciona intestinalis into oocytes of the same species to test whether these extracts can mimic the events of fertilisation. Injection of ascidian sperm extracts leads, after a delay of approximately 60 s, to a large calcium transient and repetitive pattern of calcium oscillations, mimicking the normal fertilisation response. The response was concentration-independent, suggesting a stimulatory mechanism in triggering the fertilisation response. We tested the pathway of calcium release in ascidian oocytes after injection of sperm extracts by preinjection of calcium release inhibitors. The data demonstrate that dual pathways to calcium release act at fertilisation in ascidians, as in other species. C. intestinalis oocytes are characterised by a nion channel in the plasma membrane that is gated uniquely by ADP ribose. We show that this channel is not gated by the injection of ascidian sperm extracts. Our data suggest that one metabolic pathway triggered by sperm, the release of nitric oxide, is not stimulated by sperm extracts and that several metabolic pathways are stimulated at fertilisation by more than one factor within sperm.

Spatial and temporal aspects of cell signalling

1988 ◽  
Vol 320 (1199) ◽  
pp. 325-343 ◽  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Cell Signalling ◽  
Calcium Signalling ◽  
Cell Types ◽  
Calcium Oscillations ◽  
Temporal Organization ◽  
Oscillatory Activity ◽  
Free Calcium ◽  
Inositol Lipids

As new techniques are developed to measure intracellular messengers it becomes increasingly apparent that there is a remarkable spatial and temporal organization of cell signalling. Cells possess a small discrete hormone-sensitive pool of inositol lipid. In some cells such as Xenopus oocytes and Limulus photoreceptors this phosphoinositide signalling system is highly concentrated in one region of the cell, so establishing localized calcium gradients. Another example is the hydrolysis of inositol lipids in eggs at the point of sperm entry resulting in a localized increase in Ins(1,4,5) P 3 and calcium which spreads like a wave throughout the egg. In hamster eggs this burst of calcium at fertilization recurs at 1-3 min intervals for over 100 min, a particularly dramatic example of spontaneous activity. Spontaneous oscillations in intracellular calcium exist in many different cell types and are often induced by agonists that hydrolyse inositol lipids. We have made a distinction between oscillations that are approximately sinusoidal and occur at a higher frequency where free calcium is probably continuously involved in the oscillatory cycle and those where calcium falls to resting levels for many seconds between transients. In the former case, the oscillations are thought to be induced through a cytoplasmic oscillator based on the phenomenon of calcium-induced calcium release. Such oscillations can be induced in Xenopus oocytes after injection with Ins(1,4,5) P 3 . A receptor-controlled oscillator based on the periodic formation of I ns (1,4,5) P 3 is probably responsible for the generation of the widely spaced calcium transients. The function of such calcium oscillations is currently unknown. They may be a reflection of the feedback interactions that operate to control intracellular calcium. Another possibility emerged from observations that in some cells the frequency of calcium oscillations varied with agonist concentration, suggesting that cells might employ these oscillations as a way of encoding information. One advantage of using such a frequency-dependent mechanism may lie in an increase in fidelity, especially at low agonist concentrations. Whatever these functions might be, it is clear that uncovering the mechanisms responsible for such oscillatory activity will greatly enhance our understanding of the relation between the phosphoinositides and calcium signalling.

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