Abstract
The cleavage signal transferred to the future cleavage cortex during anaphase has been proposed as 'cleavage stimulus,' but no signal has proved to induce cleavage furrows. The local Ca2+ transient along the cleavage furrow has been reported, but the Ca2+ source has remained unknown. To address these questions, we studied functions of Ca2+ stores in dividing newt eggs and found that microinjection of the Ca2+ store-enriched microsome fraction to the dividing newt egg induced a local extra-cleavage furrow at the injection site in 64-67% of the injected newt eggs while coinjection with inositol 1,4,5-trisphosphate receptor (IP3R) antagonists heparin or anti-type 1-IP3R antibody clearly suppressed this induction (5 and 11% in induction rates, respectively). Injection of cerebellar microsomes from the type 1-IP3R-deficient mice induced extracleavage furrows albeit at a low rate (19%). Our observations strongly suggest that Ca2+ stores with IP3R induce and position a cleavage furrow via IP3-induced Ca2+ release (IICR) as Ca2+-releasing machinery and putative cleavage stimulus itself.
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CITATION STYLE
Mitsuyama, F., Sawai, T., Carafoli, E., Furuichi, T., & Mikoshiba, K. (1999). Microinjection of Ca2+ store-enriched microsome fractions to dividing newt eggs induces extra-cleavage furrows via inositol 1,4,5-trisphosphate- induced Ca2+ release. Developmental Biology, 214(1), 160–167. https://doi.org/10.1006/dbio.1999.9416
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