Does cyclic ADP-ribose participate in the activation of sea urchin eggs during fertilization?

Abstract

Transient increases or oscillations of intracellular Ca²⁺concentration occur during fertilization of animal eggs from invertebrates to mammals, which is the necessary event in the egg activation. The Ca²⁺ is thought to be derived from intracellular store via inositol 1,4,5-triphosphate receptor/channel (IP3R), or via both of IP3R and ryanodine receptor/channel (RyR). The IP3R is thought to be activated by IP3 in many cell types, and to be functional in fertilization of egg cells. On the activation of RyR, the group of H.C.Lee showed that the derivative of NAD caused a Ca²⁺-transient in the egg homogenate of sea uechins in 1987, and identified cADPR as the derivative in 1989. Now it is showed that cADPR activates RyR and causes the Ca²⁺ release in many cell types. The RyR system exists in mammalian, ascidian and sea urchin eggs, but its behavior in fertilization is still unclear. The RyR is thought to be modulate by cADPR and secondarily, by a cGMP, which activates ADP-ribosyl cyclase through the action of a cGMP-dependent protein kinase to produce cADPR. We measured the cGMP, cADPR and IP3 contents of sea urchin eggs during the early stage of fertilization and compared with the Ca²⁺ rise in the presence or absence of inhibitors against guanylate cyclase. These results suggest that the RyR pathway including cGMP and cADPR is not solely responsible for the initiating the Ca²⁺-transient, but contributes to the IP3 production. [Jpn J Physiol 54 Suppl:S18 (2004)]