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J. Biol. Chem., Vol. 278, Issue 14, 12247-12254, April 4, 2003

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The NO Pathway Acts Late during the Fertilization Response in Sea Urchin Eggs^*

Calum Leckie, Ruth Empson^§, Andrea Becchetti^¶, Justyn Thomas^§, Antony Galione^§, and Michael Whitaker

From the  School of Cell and Molecular Biosciences, The Medical School, Framlington Place, University of Newcastle upon Tyne, Tyne and Wear NE2 4HH, United Kingdom, the ^§ University Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, United Kingdom

Both the inositol 1,4,5-trisphosphate (InsP₃) and ryanodine receptor pathways contribute to the Ca²⁺ transient at fertilization in sea urchin eggs. To date, the precise contribution of each pathway has been difficult to ascertain. Evidence has accumulated to suggest that the InsP₃ receptor pathway has a primary role in causing Ca²⁺ release and egg activation. However, this was recently called into question by a report implicating NO as the primary egg activator. In the present study we pursue the hypothesis that NO is a primary egg activator in sea urchin eggs and build on previous findings that an NO/cGMP/cyclic ADP-ribose (cADPR) pathway is active at fertilization in sea urchin eggs to define its role. Using a fluorescence indicator of NO levels, we have measured both NO and Ca²⁺ at fertilization and establish that NO levels rise after, not before, the Ca²⁺ wave is initiated and that this rise is Ca²⁺-dependent. By inhibiting the increase in NO at fertilization, we find not that the Ca²⁺ transient is abolished but that the duration of the transient is significantly reduced. The latency and rise time of the transient are unaffected. This effect is mirrored by the inhibition of cGMP and cADPR signaling in sea urchin eggs at fertilization. We establish that cADPR is generated at fertilization, at a time comparable to the time of the rise in NO levels. We conclude that NO is unlikely to be a primary egg activator but, rather, acts after the initiation of the Ca²⁺ wave to regulate the duration of the fertilization Ca²⁺ transient.

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