scholarly journals Differential regulation of nicotinic acid–adenine dinucleotide phosphate and cADP-ribose production by cAMP and cGMP

1998 ◽  
Vol 331 (3) ◽  
pp. 837-843 ◽  
Author(s):  
Heather L. WILSON ◽  
Antony GALIONE
Keyword(s):  
Nicotinic Acid ◽  
Sea Urchin ◽  
Calcium Release ◽  
Second Messengers ◽  
Differential Regulation ◽  
Sea Urchin Egg ◽  
Inositol 1,4,5 Trisphosphate ◽  
Extracellular Stimuli ◽  
Camp And Cgmp ◽  
Temperature Optima

The sea urchin egg has been used as a system to study calcium-release mechanisms induced by inositol 1,4,5-trisphosphate (IP3), cADP-ribose (cADPR), and more recently, nicotinic acid–adenine dinucleotide phosphate (NAADP). In order that cADPR and NAADP may be established as endogenous messengers for calcium release, the existence of intracellular enzymes capable of metabolizing these molecules must be demonstrated. In addition, intracellular levels of cADPR and NAADP should be under the control of extracellular stimuli. It has been shown that cGMP stimulates the synthesis of cADPR in the sea urchin egg. The present study shows that the sea urchin egg is capable of synthesizing and degrading NAADP. cADPR and NAADP synthetic activities appear to be separate, with different cellular localizations, pH and temperature optima. We suggest that in the sea urchin egg, cADPR and NAADP production may be differentially regulated by receptor-coupled second messengers, with cADPR production being regulated by cGMP and NAADP production modulated by cAMP.

scholarly journals Nicotinic acid-adenine dinucleotide phosphate mobilizes Ca2+ from a thapsigargin-insensitive pool

1996 ◽  
Vol 315 (3) ◽  
pp. 721-725 ◽  
Author(s):  
Armando A. GENAZZANI ◽  
Antony GALIONE
Keyword(s):  
Nicotinic Acid ◽  
Sea Urchin ◽  
Cross Talk ◽  
Inositol Trisphosphate ◽  
Sea Urchin Eggs ◽  
Bivalent Cations ◽  
Sea Urchin Egg ◽  
Different Characteristics ◽  
Degree Of Overlap

Nicotinic acid–adenine dinucleotide phosphate (NAADP) is a novel intracellular Ca2+ releasing agent recently described in sea-urchin eggs and egg homogenates. Ca2+ release by NAADP is independent of that induced by either inositol trisphosphate (InsP3) or cyclic adenosine dinucleotide phosphate (cADPR). We now report that in sea urchin egg homogenates, NAADP releases Ca2+ from a Ca2+ pool that is distinct from those that are sensitive to InsP3 and cADPR. This organelle has distinct Ca2+ uptake characteristics: it is insensitive to thapsigargin and cyclopiazoic acid, but maintenance of the pool shows some requirement for ATP. Although the different Ca2+ pools have different characteristics, there appears to be some degree of overlap or cross-talk between the NAADP- and cADPR/InsP3-sensitive Ca2+ pools. Ca2+-induced Ca2+ release is unlikely to account for the apparent overlap between stores, since NAADP-induced Ca2+ release, in contrast with that stimulated by cADPR, is not potentiated by bivalent cations.

scholarly journals Ca2+ release triggered by NAADP in hepatocyte microsomes

2006 ◽  
Vol 395 (2) ◽  
pp. 233-238 ◽  
Author(s):  
Miklós Mándi ◽  
Balázs Tóth ◽  
György Timár ◽  
Judit Bak
Keyword(s):  
Nicotinic Acid ◽  
Ryanodine Receptor ◽  
Sea Urchin ◽  
Mammalian Cells ◽  
Liver Microsomes ◽  
The Other ◽  
Release Mechanism ◽  
Ip3 Receptors ◽  
Rat Hepatocyte ◽  
Inositol 1,4,5 Trisphosphate

NAADP (nicotinic acid–adenine dinucleotide phosphate) is fast emerging as a new intracellular Ca2+-mobilizing messenger. NAADP induces Ca2+ release by a mechanism that is distinct from IP3 (inositol 1,4,5-trisphosphate)- and cADPR (cADP-ribose)-induced Ca2+ release. In the present study, we demonstrated that micromolar concentrations of NAADP trigger Ca2+ release from rat hepatocyte microsomes. Cross-desensitization to IP3 and cADPR by NAADP did not occur in liver microsomes. We report that non-activating concentrations of NAADP can fully inactivate the NAADP-sensitive Ca2+-release mechanism in hepatocyte microsomes. The ability of thapsigargin to block the NAADP-sensitive Ca2+ release is not observed in sea-urchin eggs or in intact mammalian cells. In contrast with the Ca2+ release induced by IP3 and cADPR, the Ca2+ release induced by NAADP was completely independent of the free extravesicular Ca2+ concentration and pH (in the range 6.4–7.8). The NAADP-elicited Ca2+ release cannot be blocked by the inhibitors of the IP3 receptors and the ryanodine receptor. On the other hand, verapamil and diltiazem do inhibit the NAADP- (but not IP3- or cADPR-) induced Ca2+ release.

Psammechinus miliaris egg homogenate as a model to investigate Ca2+-release mechanisms

1999 ◽  
Vol 79 (2) ◽  
pp. 323-326 ◽  
Author(s):  
Armando A. Genazzani ◽  
Heather L. Wilson ◽  
Antony Galione
Keyword(s):  
Sea Urchin ◽  
Calcium Release ◽  
Lytechinus Pictus ◽  
Release Mechanisms ◽  
Psammechinus Miliaris ◽  
Sea Urchin Egg ◽  
Cyclic Adp Ribose ◽  
The Usa ◽  
Release Model ◽  
Convenient Model

The sea urchin egg has proved a reliable and robust system for measuring intracellular calcium release in response to three independent mechanisms: inositol 1,4,5 trisphosphate, cyclic ADP-ribose and the recently identified molecule, nicotinic acid adenine dinucleotide phosphate (NAADP). These calcium release mechanisms have been studied in homogenates of Lytechinus pictus and Spongylocentrotus purpuratus, which are two sea urchin species located off the west coast of the USA. A new calcium-release model from a species of sea urchin present off the coasts of Britain, Psammechinus miliaris is characterized and described. Although the Ca2+-release characteristics in this species do not differ from those of the other two sea urchin species, it may provide a more economical and convenient model for European scientists.

scholarly journals Photoaffinity Labeling of High Affinity Nicotinic Acid Adenine Dinucleotide Phosphate (NAADP)-Binding Proteins in Sea Urchin Egg

2011 ◽  
Vol 287 (4) ◽  
pp. 2308-2315 ◽  
Author(s):  
Timothy F. Walseth ◽  
Yaping Lin-Moshier ◽  
Pooja Jain ◽  
Margarida Ruas ◽  
John Parrington ◽  
...  
Keyword(s):  
Nicotinic Acid ◽  
Sea Urchin ◽  
Binding Proteins ◽  
Photoaffinity Labeling ◽  
High Affinity ◽  
Sea Urchin Egg

scholarly journals Unique kinetics of nicotinic acid–adenine dinucleotide phosphate (NAADP) binding enhance the sensitivity of NAADP receptors for their ligand

2000 ◽  
Vol 352 (3) ◽  
pp. 725-729 ◽  
Author(s):  
Sandip PATEL ◽  
Grant C. CHURCHILL ◽  
Antony GALIONE
Keyword(s):  
Nicotinic Acid ◽  
Sea Urchin ◽  
Binding Sites ◽  
Cell Types ◽  
Unique Property ◽  
Single Class ◽  
High Affinity ◽  
Sea Urchin Egg ◽  
Low Concentrations ◽  
Kinetics Of

Nicotinic acidŐadenine dinucleotide phosphate (NAADP) is a novel and potent Ca2+-mobilizing agent in sea urchin eggs and other cell types. Little is known, however, concerning the properties of the putative intracellular NAADP receptor. In the present study we have characterized NAADP binding sites in sea urchin egg homogenates. [32P]NAADP bound to a single class of high-affinity sites that were reversibly inhibited by NaCl but insensitive to pH and Ca2+. Binding of [32P]NAADP was lost in preparations that did not mobilize Ca2+ in response to NAADP, indicating that [32P]NAADP probably binds to a receptor mediating Ca2+ mobilization. Addition of excess unlabelled NAADP, at various times after initiation of [32P]NAADP binding, did not result in displacement of bound [32P]NAADP. These data show that NAADP becomes irreversibly bound to its receptor immediately upon association. Accordingly, incubation of homogenates with low concentrations of NAADP resulted in maximal labelling of NAADP binding sites. This unique property renders NAADP receptors exquisitely sensitive to their ligand, thereby allowing detection of minute changes in NAADP levels.

scholarly journals Cortical localization of a calcium release channel in sea urchin eggs.

1992 ◽  
Vol 116 (5) ◽  
pp. 1111-1121 ◽  
Author(s):  
S M McPherson ◽  
P S McPherson ◽  
L Mathews ◽  
K P Campbell ◽  
F J Longo
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptor ◽  
Sea Urchin ◽  
Calcium Release ◽  
Staining Pattern ◽  
Cortical Granule ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Sea Urchin Eggs ◽  
Sea Urchin Egg

We have used an antibody against the ryanodine receptor/calcium release channel of skeletal muscle sarcoplasmic reticulum to localize a calcium release channel in sea urchin eggs. The calcium release channel is present in less than 20% of immature oocytes, where it does not demonstrate a specific cytoplasmic localization, while it is confined to the cortex of all mature eggs examined. This is in contrast to the cortical and subcortical localization of calsequestrin in mature and immature eggs. Immunolocalization of the calcium release channel reveals a cortical reticulum or honeycomb staining network that surrounds cortical granules and is associated with the plasma membrane. The network consists of some immunoreactive electron-dense material coating small vesicles and elongate cisternae of the endoplasmic reticulum. The fluorescent reticular staining pattern is lost when egg cortices are treated with agents known to affect sarcoplasmic reticulum calcium release and induce cortical granule exocytosis (ryanodine, calcium, A-23187, and caffeine). An approximately 380-kD protein of sea urchin egg cortices is identified by immunoblot analysis with the ryanodine receptor antibody. These results demonstrate: (a) the presence of a ryanodine-sensitive calcium release channel that is located within the sea urchin egg cortex; (b) an altered calcium release channel staining pattern as a result of treatments that initiate the cortical granule reaction; and (c) a spatial and functional dichotomy of the ER which may be important in serving different roles in the mobilization of calcium at fertilization.

scholarly journals Ca2+ release triggered by nicotinate adenine dinucleotide phosphate in intact sea urchin eggs

1995 ◽  
Vol 312 (3) ◽  
pp. 955-959 ◽  
Author(s):  
C M Perez-Terzic ◽  
E N Chini ◽  
S S Shen ◽  
T P Dousa ◽  
D E Clapham
Keyword(s):  
Sea Urchin ◽  
Specific Inhibitor ◽  
Intact Cells ◽  
Sea Urchin Eggs ◽  
Sea Urchin Egg ◽  
Cyclic Adp Ribose ◽  
Inositol 1,4,5 Trisphosphate ◽  
Dose Dependent Increase ◽  
Dose Dependent

Nicotinate adenine dinucleotide phosphate (NAADP) was recently identified [Lee and Aarhus (1995) J. Biol. Chem. 270, 2152-2157; Chini, Beers and Dousa (1995) J. Biol. Chem. 270, 3116-3223] as a potent Ca(2+)-releasing agent in sea urchin egg homogenates. NAADP triggered Ca2+ release by a mechanism that was distinct from inositol 1,4,5-trisphosphate (InsP3)- and cyclic ADP-ribose (cADPR)-induced Ca2+ release. When NAADP was microinjected into intact sea urchin eggs it induced a dose-dependent increase in cytoplasmic free Ca2+ which was independent of the extracellular [Ca2+]. The Ca2+ waves elicited by microinjections of NAADP originated at the site of injection and swept across the cytosol. As previously found in sea urchin egg homogenates, NAADP-induced Ca2+ release in intact eggs was not blocked by heparin or by prior desensitization to InsP3 or cADPR. Thio-NADP, a specific inhibitor of the NAADP-induced Ca2+ release in sea urchin homogenates [Chini, Beers and Dousa (1995) J. Biol. Chem. 270, 3116-3223] blocked NAADP (but not InsP3 or cADPR) injection-induced Ca2+ release in intact sea urchin eggs. Finally, fertilization of sea urchin eggs abrogated subsequent NAADP-induced Ca2+ release, suggesting that the NAADP-sensitive Ca2+ pool may participate in the fertilization response. This study demonstrates that NAADP acts as a selective Ca(2+)-releasing agonist in intact cells.

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