scholarly journals The Cyclic GMP-Mediated Calcium Release Pathway in Sea Urchin Eggs Is Not Required for the Rise in Calcium during Fertilization

1996 ◽  
Vol 180 (1) ◽  
pp. 324-335 ◽  
Author(s):  
Shyh-Jye Lee ◽  
Leslie Christenson ◽  
Tracie Martin ◽  
Sheldon S. Shen
Keyword(s):  
Sea Urchin ◽  
Cyclic Gmp ◽  
Calcium Release ◽  
Sea Urchin Eggs

scholarly journals Calcium- and polyphosphate-containing acidic granules of sea urchin eggs are similar to acidocalcisomes, but are not the targets for NAADP

2010 ◽  
Vol 429 (3) ◽  
pp. 485-495 ◽  
Author(s):  
Isabela B. Ramos ◽  
Kildare Miranda ◽  
Douglas A. Pace ◽  
Katherine C. Verbist ◽  
Fu-Yang Lin ◽  
...  
Keyword(s):  
Sea Urchin ◽  
31P Nmr ◽  
Calcium Release ◽  
High Energy ◽  
Bafilomycin A1 ◽  
X Ray ◽  
Sea Urchin Eggs ◽  
Calcium Storage ◽  
Granule Fraction ◽  
Sodium Magnesium

Acidocalcisomes are acidic calcium-storage compartments described from bacteria to humans and characterized by their high content in poly P (polyphosphate), a linear polymer of many tens to hundreds of Pi residues linked by high-energy phosphoanhydride bonds. In the present paper we report that millimolar levels of short-chain poly P (in terms of Pi residues) and inorganic PPi are present in sea urchin extracts as detected using 31P-NMR, enzymatic determinations and agarose gel electrophoresis. Poly P was localized to granules randomly distributed in the sea urchin eggs, as shown by labelling with the poly-P-binding domain of Escherichia coli exopolyphosphatase. These granules were enriched using iodixanol centrifugation and shown to be acidic and to contain poly P, as determined by Acridine Orange and DAPI (4′,6′-diamidino-2-phenylindole) staining respectively. These granules also contained large amounts of calcium, sodium, magnesium, potassium and zinc, as detected by X-ray microanalysis, and bafilomycin A1-sensitive ATPase, pyrophosphatase and exopolyphosphatase activities, as well as Ca2+/H+ and Na+/H+ exchange activities, being therefore similar to acidocalcisomes described in other organisms. Calcium release from these granules induced by nigericin was associated with poly P hydrolysis. Although NAADP (nicotinic acid–adenine dinucleotide phosphate) released calcium from the granule fraction, this activity was not significantly enriched as compared with the NAADP-stimulated calcium release from homogenates and was not accompanied by poly P hydrolysis. GPN (glycyl-L-phenylalanine-naphthylamide) released calcium when added to sea urchin homogenates, but was unable to release calcium from acidocalcisome-enriched fractions, suggesting that these acidic stores are not the targets for NAADP.

U73122 Blocked the cGMP-Induced Calcium Release in Sea Urchin Eggs

1998 ◽  
Vol 242 (1) ◽  
pp. 328-340 ◽  
Author(s):  
Shyh-Jye Lee ◽  
Patrick J. Madden ◽  
Sheldon S. Shen
Keyword(s):  
Sea Urchin ◽  
Calcium Release ◽  
Sea Urchin Eggs

NAADP-induced calcium release in sea urchin eggs

2000 ◽  
Vol 92 (3-4) ◽  
pp. 197-204 ◽  
Author(s):  
Antony Galione ◽  
Sandip Patel ◽  
Grant C. Churchill
Keyword(s):  
Sea Urchin ◽  
Calcium Release ◽  
Sea Urchin Eggs

scholarly journals Evidence That Src-Type Tyrosine Kinase Activity Is Necessary for Initiation of Calcium Release at Fertilization in Sea Urchin Eggs

2000 ◽  
Vol 218 (2) ◽  
pp. 206-219 ◽  
Author(s):  
Yama A. Abassi ◽  
David J. Carroll ◽  
Andrew F. Giusti ◽  
Robert J. Belton ◽  
Kathy R. Foltz
Keyword(s):  
Tyrosine Kinase ◽  
Sea Urchin ◽  
Calcium Release ◽  
Kinase Activity ◽  
Tyrosine Kinase Activity ◽  
Sea Urchin Eggs

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 Thimerosal reveals calcium-induced calcium release in unfertilised sea urchin eggs

Zygote ◽  
1993 ◽  
Vol 1 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Alex McDougall ◽  
Isabelle Gillot ◽  
Michael Whitaker
Keyword(s):  
Sea Urchin ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Transient ◽  
Cell Types ◽  
Egg Activation ◽  
Free Calcium ◽  
Slow Increase ◽  
Sea Urchin Eggs ◽  
Calcium Induced Calcium Release

SummaryThe fertilisation calcium wave in sea urchin eggs triggers the onset of development. The wave is an explosive increase in intracellular free calcium concentration that begins at the point of sperm entry and crosses the egg in about 20 s. Thimerosal is a sulphydryl reagent that sensitises calcium release from intracellular stores in a variety of cell types. Treatment of unfertilised eggs with thimerosal causes a slow increase that results eventually in a large, spontaneous calcium transient and egg activation. At shorter times after thimerosal treatment, egg activation and the calcium transient can be triggered by calcium influx through voltage-gated calcium channels, a form of calcium-induced/calcium release (CICR). Thimerosal treatment also reduces the latency of the fertilisation calcium response and increases the velocity of the fertilisation wave. These results indicate that thimerosal can unmask CICR in sea urchin eggs and suggest that the ryanodine receptor channel based CICR may contribute to explosive calcium release during the fertilisation wave.

scholarly journals Internal calcium release and activation of sea urchin eggs by cGMP are independent of the phosphoinositide signaling pathway.

1992 ◽  
Vol 3 (3) ◽  
pp. 373-383 ◽  
Author(s):  
T Whalley ◽  
A McDougall ◽  
I Crossley ◽  
K Swann ◽  
M Whitaker
Keyword(s):  
Signaling Pathway ◽  
Sea Urchin ◽  
Calcium Release ◽  
Ion Concentration ◽  
Free Calcium ◽  
Calcium Stores ◽  
Phosphoinositide Signaling ◽  
Sea Urchin Eggs ◽  
Calcium Ion Concentration ◽  
Internal Calcium

We show that microinjecting cyclic GMP (cGMP) into unfertilized sea urchin eggs activates them by stimulating a rise in the intracellular free calcium ion concentration ([Ca2+]i). The increase in [Ca2+]i is similar in both magnitude and duration to the transient that activates the egg at fertilization. It is due to mobilization of calcium from intracellular stores but is not prevented by the inositol trisphosphate (InsP3) antagonist heparin. Furthermore, cGMP does not stimulate the eggs Na+/H+ antiport when the [Ca2+]i transient is blocked by the calcium chelator bis-(O-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA), suggesting that cGMP does not activate eggs by interacting with the their phosphoinositide signaling pathway. However, the [Ca2+]i increase and activation are prevented in eggs in which the InsP3-sensitive calcium stores have been emptied by the prior microinjection of the InsP3 analogue inositol 1,4,5-trisphosphorothioate. These data indicate that cGMP activates eggs by stimulating the release of calcium from an InsP3-sensitive calcium store via a novel, though unidentified, route independent of the InsP3 receptor.

Cortical granule exocytosis is triggered by different thresholds of calcium during fertilisation in sea urchin eggs

Zygote ◽  
1998 ◽  
Vol 6 (1) ◽  
pp. 55-63 ◽  
Author(s):  
John C. Matese ◽  
David R. McClay
Keyword(s):  
Plasma Membrane ◽  
Sea Urchin ◽  
Calcium Release ◽  
Threshold Concentration ◽  
Calcium Wave ◽  
Cortical Granule ◽  
Cortical Granules ◽  
Granule Exocytosis ◽  
Sea Urchin Eggs ◽  
Cortical Granule Exocytosis

SummaryIn sea urchin eggs, fertilisation is followed by a calcium wave, cortical granule exocytosis and fertilisation envelope elevation. Both the calcium wave and cortical granule exocytosis sweep across the egg in a wave initiated at the point of sperm entry. Using differential interference contrast (DIC) microscopy combined with laser scanning confocal microscopy, populations of cortical granules undergoing calcium-induced exocytosis were observed in living urchin eggs. Calcium imaging using the indicator Calcium Green-dextran was combined with an image subtraction technique for visual isolation of individual exocytotic events. Relative fluorescence levels of the calcium indicator during the fertilisation wave were compared with cortical fusion events. In localised regions of the egg, there is a 6s delay between the detection of calcium release and fusion of cortical granules. The rate of calcium accumulation was altered experimentally to ask whether this delay was necessary to achieve a threshold concentration of calcium to trigger fusion, or was a time-dependent activation of the cortical granule fusion apparatus after the ‘triggering’ event. Calcium release rate was attenuated by blocking inositol 1,4,5-triphospate (InsP3)-gated channels with heparin. Heparin extended the time necessary to achieve a minimum concentration of calcium at the sites of cortical granule exocytosis. The data are consistent with the conclusion that much of the delay observed normally is necessary to reach threshold concentration of calcium. Cortical granules then fuse with the plasma membrane. Further, once the minimum threshold calcium concentration is reached, cortical granule fusion with the plasma membrane occurs in a pattern suggesting that cortical granules are non-uniform in their calcium sensitivity threshold.

Sign in / Sign up

Export Citation Format

Share Document