Ciapa B, Pesando D, Wilding M, Whitaker M
Laboratoire de Physiologie Cellulaire et Comparée, Faculté des Sciences, Nice, France.
Nature. 1994 Apr 28;368(6474):875-8. doi: 10.1038/368875a0.
Transient changes in intracellular calcium ([Ca2+]i) have been shown to punctuate the cell cycle in various types of cells in culture and in early embryos. The [Ca2+]i transients are correlated with cell-cycle events: pronuclear migration, nuclear envelope breakdown, the metaphase-anaphase transition of mitosis, and cytokinesis. Mitotic events can be induced by injecting calcium and prevented by injecting calcium chelators into the sea urchin embryo. Cell-cycle calcium transients differ from the transients linked to membrane signal transduction pathways: they are generated by an endogenous mechanism, not by plasma membrane receptor complexes, and their trigger is unknown. We report here that the phosphoinositide messenger system oscillates during the early embryonic cell cycle in the sea urchin, leading to cyclic increases in inositol trisphosphate that trigger cell-cycle [Ca2+]i transients and mitosis by calcium release from intracellular stores.
细胞内钙（[Ca2+]i）的瞬时变化已被证明在培养的各种细胞类型和早期胚胎中贯穿细胞周期。[Ca2+]i瞬时变化与细胞周期事件相关：原核迁移、核膜破裂、有丝分裂的中期-后期转换以及胞质分裂。通过向海胆胚胎注射钙可以诱导有丝分裂事件，而注射钙螯合剂则可以阻止这些事件。细胞周期钙瞬变不同于与膜信号转导途径相关的瞬变：它们是由内源性机制产生的，而非质膜受体复合物，并且其触发因素尚不清楚。我们在此报告，磷脂酰肌醇信使系统在海胆早期胚胎细胞周期中振荡，导致肌醇三磷酸的周期性增加，通过从细胞内储存中释放钙来触发细胞周期[Ca2+]i瞬变和有丝分裂。
