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The involvement of Ca2+ in the activation of eggs and in the first steps of the embryonic development of several species is a well-known phenomenon. An association between Ca2+ sources with the fate of the blastopore during embryonic development has been investigated by several authors. Ca2+ influx mediated by voltage-gated channels and Ca2+ mobilization from intracellular stores are the major sources of Ca2+ to egg activation and succeeding cell divisions. Studies on sea urchins embryonic development show that intracellular Ca2+ stores are responsible for egg activation and early embryogenesis. In the present work we investigated the involvement of extracellular Ca2+ in the first stages of the embryonic development of the sea urchin Echinometra lucunter. Divalent cation chelators EDTA and EGTA strongly blocked the early embryonic development. Adding to this, we demonstrated the involvement of voltage-gated Ca2+ channels in E. lucunter embryogenesis since Ca2+ channel blockers powerfully inhibited the early embryonic development. Our data also revealed that Ca2+ influx is crucial for embryonic development during only the first 40 min postfertilization. However, intracellular Ca2+ remains mandatory to embryonic development 40 min postfertilization, seen that both the intracellular Ca2+ chelator BAPTA-AM and calmodulin antagonists trifluoperazine and chlorpromazine inhibited the first stages of development when added to embryos culture 50 min postfertilization. Our work highlights the crucial role of extracellular Ca2+ influx through voltage-gated Ca2+ channels for the early embryonic development of the sea urchin E. lucunter and characterizes an exception in the phylum Echinodermata. J. Exp. Zool. (Mol. Dev. Evol.) 318:123–133, 2012. © 2011 Wiley Periodicals, Inc.