- Title
- A cell cycle-associated change in Ca²⁺ releasing activity leads to the generation of Ca²⁺ transients in mouse embryos during the first mitotic division
- Creator
- Kono, Tomohiro; Jones, Keith T.; Bos-Mikich, Adriana; Whittingham, David G.; Carroll, John
- Relation
- Journal of Cell Biology Vol. 132, Issue 5, p. 5915-5923
- Publisher Link
- http://dx.doi.org/10.1083/jcb.132.5.915
- Publisher
- Rockefeller University Press
- Resource Type
- journal article
- Date
- 1996
- Description
- We have used Ca²⁺-sensitive fluorescent dyes to monitor intracellular Ca²⁺ during mitosis in one-cell mouse embryos. We find that fertilized embryos generate Ca²⁺ transients at nuclear envelope breakdown (NEBD) and during mitosis. In addition, fertilized embryos arrested in metaphase using colcemid continue to generate Ca²⁺ transients. In contrast, parthenogenetic embryos produced by a 2-h exposure to strontium containing medium do not generate detectable Ca²⁺ transients at NEBD or in mitosis. However, when parthenogenetic embryos are cultured continuously in strontium containing medium Ca²⁺ transients are detected in mitosis but not in interphase. This suggests that mitotic Ca²⁺ transients are detected in the presence of an appropriate stimulus such as fertilization or strontium. The Ca²⁺ transient detected in fertilized embryos is not necessary for inducing NEBD since parthenogenetic embryos undergo nuclear envelope breakdown (NEBD). Also the first sign that NEBD is imminent occurs several minutes before the Ca²⁺ transient. The Ca²⁺ transient at NEBD appears to be associated with the nucleus since nuclear transfer experiments show that the presence of a karyoplast from a fertilized embryo is essential. Finally, we show that the intracellular Ca²⁺ chelator Bapta inhibits NEBD in fertilized and parthenogenetic embryos in a dose-dependent manner. These studies show that during mitosis there is an endogenous increase in Ca²⁺ releasing activity that leads to the generation of Ca²⁺ transients specifically during mitosis. The ability of Ca²⁺ buffers to inhibit NEBD regardless of the presence of global Ca²⁺ transients suggests that the underlying cell cycle-associated Ca²⁺ releasing activity may take the form of localized Ca²⁺ transients.
- Subject
- Ca²⁺; embryos; mitosis; mouse; mitotic
- Identifier
- http://hdl.handle.net/1959.13/804180
- Identifier
- uon:6547
- Identifier
- ISSN:0021-9525
- Language
- eng
- Full Text
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