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Translational control of InsP3-induced chromatin condensation during the early cell cycles of sea urchin embryos

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Abstract

The cycles of DNA synthesis and chromatin condensation in dividing cells are controlled by signals from the cytoplasm1–3. Changes in the concentration of free calcium (Cai) in the cytoplasm control a variety of cellular functions4 and it has thus been suggested that observed variations in Cai during the cell cycle may be the cytoplas-mic signal that co-ordinates nuclear and cytoplasmic division5–9. We show here that increases in Cai induced by the calcium-releasing second messenger inositol 1,4,5-triphosphate (Ins(l,4,5)P3), or by calcium buffers, cause premature chromatin condensation and breakdown of the nuclear envelope in sea urchin (Lytechinus pictus) early embryos. Both natural and induced chromatin condensation are prevented by calcium chelators. The nucleus becomes sensitive to the Cai signal 45 min after fertilization, but remains insensitive if protein synthesis is prevented. Our experiments demonstrate that Cai regulates the behaviour of the nucleus during the cell cycle, suggest that Ins(l,4,5)P3 is a cell cycle messenger and indicate that there is an interaction between the protein and ionic signals that control the state of chromatin during the cell cycle.

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Twigg, J., Patel, R. & Whitaker, M. Translational control of InsP3-induced chromatin condensation during the early cell cycles of sea urchin embryos. Nature 332, 366–369 (1988). https://doi.org/10.1038/332366a0

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