ArticleThe Journal of cell biology1996
A cell cycle-associated change in Ca2+ releasing activity leads to the generation of Ca2+ transients in mouse embryos during the first mitotic division.
Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 101 citations in OpenAlex.
- Targeting EGFR-REM2-CaCellular and molecular life sciences : CMLS · 2025Article
- Dynamic shapes of the zygote and two-cell mouse and human.Biology open · 2021Article
- CaCold Spring Harbor perspectives in biology · 2019Review
- A novel mutation in the TUBB8 gene is associated with complete cleavage failure in fertilized eggs.Journal of assisted reproduction and genetics · 2018Article
- Signal transduction in mammalian oocytes during fertilization.Cell and tissue research · 2016Review
- The effects of calcitonin on the development of and Ca2+ levels in heat-shocked bovine preimplantation embryos in vitro.The Journal of reproduction and development · 2014Article
- TRPV3 channels mediate strontium-induced mouse-egg activation.Cell reports · 2013Article
- Calcium signaling in mammalian egg activation and embryo development: the influence of subcellular localization.Molecular reproduction and development · 2012Review
- Downregulation of H19 improves the differentiation potential of mouse parthenogenetic embryonic stem cells.Stem cells and development · 2012Article
- Ca2+ signaling during mammalian fertilization: requirements, players, and adaptations.Cold Spring Harbor perspectives in biology · 2011Review
- Expression of calbindin-D28k and its regulation by estrogen in the human endometrium during the menstrual cycle.Reproductive biology and endocrinology : RB&E · 2011Article
- Expression of stemness markers in mouse parthenogenetic-diploid blastocysts is influenced by slight variation of activation protocol adopted.In vitro cellular & developmental biology. Animal · 2010Article
- The present status of artificial oocyte activation in assisted reproductive technology.Reproductive medicine and biology · 2008Review
- Calcium signalling in early embryos.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2008Review
- Phosphorylation of IP3R1 and the regulation of [Ca2+]i responses at fertilization: a role for the MAP kinase pathway.Development (Cambridge, England) · 2006Article
- Mouse Emi2 is required to enter meiosis II by reestablishing cyclin B1 during interkinesis.The Journal of cell biology · 2006Article
- Calcium at fertilization and in early development.Physiological reviews · 2006Review
- Inhibiting MAP kinase activity prevents calcium transients and mitosis entry in early sea urchin embryos.The Journal of biological chemistry · 2005Article
- Cell cycle-dependent regulation of structure of endoplasmic reticulum and inositol 1,4,5-trisphosphate-induced Ca2+ release in mouse oocytes and embryos.Molecular biology of the cell · 2003Article
- Effects of temperature on calcium-sensitive fluorescent probes.Biophysical journal · 2000Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.