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Cell-cycle calcium transients driven by cyclic changes in inositol trisphosphate levels

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Abstract

TRANSIENT changes in intracellular calcium ([Ca2+]i) have been shown to punctuate the cell cycle in various types of cells in culture1–5 and in early embryos6–12. 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 can be induced by injecting calcium and prevented by injecting calcium chelators into the sea urchin embryo10,13. 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.

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Ciapa, B., Pesando, D., Wilding, M. et al. Cell-cycle calcium transients driven by cyclic changes in inositol trisphosphate levels. Nature 368, 875–878 (1994). https://doi.org/10.1038/368875a0

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