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Echinobase
ECB-ART-31036
Mol Biol Cell 1992 Mar 01;33:373-83. doi: 10.1091/mbc.3.3.373.
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Internal calcium release and activation of sea urchin eggs by cGMP are independent of the phosphoinositide signaling pathway.

Whalley T , McDougall A , Crossley I , Swann K , Whitaker M .


Abstract
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.

PubMed ID: 1320962
PMC ID: PMC275537
Article link: Mol Biol Cell
Grant support: [+]

Genes referenced: LOC100887844

References [+] :
ALLEN, The time sequence of early events in the fertilization of sea urchin eggs. I. The latent period and the cortical reaction. 1958, Pubmed, Echinobase