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NAADP‐induced calcium release in sea urchin eggs
Author(s) -
Galione Antony,
Patel Sandip,
Churchill Grant C.
Publication year - 2000
Publication title -
biology of the cell
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.543
H-Index - 85
eISSN - 1768-322X
pISSN - 0248-4900
DOI - 10.1016/s0248-4900(00)01070-4
Subject(s) - ryanodine receptor , biology , sea urchin , intracellular , thapsigargin , microbiology and biotechnology , endoplasmic reticulum , inositol trisphosphate receptor , inositol trisphosphate , calcium signaling , activator (genetics) , voltage dependent calcium channel , biophysics , cyclic adp ribose , calcium , inositol , biochemistry , receptor , chemistry , cd38 , stem cell , organic chemistry , cd34
Nicotinic acid adenine dinucleotide phosphate (NAADP) is the most potent activator of Ca 2+ release from intracellular stores described. It acts on a mechanism distinct from inositol trisphosphate and ryanodine receptors, the two major Ca 2+ release channels characterised. NAADP‐gated Ca 2+ release channels do not appear to be regulated by Ca 2+ and may be better suited for triggering Ca 2+ signals rather than propagating them. They exhibit a remarkable pharmacology for a putative intracellular Ca 2+ release channel in that they are selectively blocked by potassium and L‐type Ca 2+ channel antagonists. Furthermore, in contrast to microsomal Ca 2+ stores expressing IP 2+ Rs and RyRs, those sensitive to NAADP are thapsigargin‐insensitive, suggesting that they may be expressed on a different part of the endoplasmic reticulum. Perhaps the most unusual feature of the NAADP‐gated Ca 2+ release mechanisms is its inactivation properties. Unlike the mechanisms regulated by IP 2+ and cADPR in sea urchin eggs which after induction of Ca 2+ release appear to become refractory to subsequent activation, very low concentrations of NAADP are able to inactivate NAADP‐induced Ca 2+ release fully at concentrations well below those required to activate Ca 2+ release. The mechanism and physiological significance of this most unusual desensitisation phenomenon are unclear. More recently, NAADP has been shown to mobilise Ca 2+ in ascidian oocytes, brain microsomes and pancreatic acinar cells suggesting a more widespread role in Ca 2+ signalling. A possible role for this novel Ca 2+ release mechanism in sea urchin egg fertilisation is discussed.