CELL-CYCLE CALCIUM TRANSIENTS DRIVEN BY CYCLIC CHANGES IN INOSITOL TRISPHOSPHATE LEVELS
CELL-CYCLE CALCIUM TRANSIENTS DRIVEN BY CYCLIC CHANGES IN INOSITOL TRISPHOSPHATE LEVELS
复制标题
由三磷酸肌醇水平周期性变化驱动的细胞周期钙离子瞬变
DOI：
10.1038/368875a0
复制
发表时间：
1994-04-28
期刊：
影响因子：
64.8
通讯作者：
WHITAKER, M
中科院分区：
文献类型：
--
作者：
CIAPA, B;PESANDO, D;WHITAKER, M
细胞内钙离子（[Ca 2 +]（i））的瞬时变化已被证明会打断培养物（1-5）和早期胚胎（6-12）中各种类型细胞的细胞周期。[Ca 2 +]（i）瞬变与细胞周期事件相关：原核迁移、核膜破裂、有丝分裂的中期-后期转换和胞质分裂。有丝分裂事件可以通过向海胆胚胎注射钙来诱导，并通过向海胆胚胎注射钙螯合剂来预防（10，13）。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，而不是由质膜受体复合物产生的，并且它们的触发机制未知。我们在这里报告，磷脂酰肌醇信使系统振荡在早期胚胎细胞周期的海胆，导致周期性增加肌醇三磷酸，触发细胞周期[Ca 2 +]（i）瞬变和有丝分裂的钙释放从细胞内存储。
TRANSIENT changes in intracellular calcium ([Ca2+](i)) have been shown to punctuate the cell cycle in various types of cells in culture(1-5) and in early embryos(6-12). 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 fan be induced by injecting calcium and prevented by injecting calcium chelators into the sea urchin embryo(10,13). 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.