Regulation of fertilization-induced Ca(2+)spiking in the mouse zygote

• Published in: Cell calcium (Edinburgh) 2000-07, Vol.28 (1), p.47-54
• Main Authors: Day, M L, McGuinness, O M, Berridge, M J, Johnson, M H
• Format: Article
• Language: English
• Subjects: Animals; Calcium Signaling; Cell Cycle; Cell Nucleus - physiology; Dithiothreitol - pharmacology; Fertilization; Mice; Oxidation-Reduction - drug effects; Zygote - metabolism
• ISSN: 0143-4160
• DOI: 10.1054/ceca.2000.0128

Fertilization-induced Ca(2+)spiking in mouse zygotes ceases at the end of pre-G1 as pronuclei (PN) form. In the present studies we found that there was no consistent temporal relationship between PN formation and cessation of spiking. We also show that nucleate and anucleate fragments of zygotes, obtained by bisection of fertilized eggs prior to PN formation, both ceased spiking at times that did not depend on the presence of the PN. We, therefore, concluded that formation of the PN does not cause spiking cessation. The possibility that cessation of the fertilization-induced Ca(2+)spiking may be mediated by a redox sensitive mechanism affecting the sensitivity of Ca(2+)release from internal stores is proposed. At first mitosis, a small proportion of zygotes show low amplitude calcium spikes prior to pronuclear envelope breakdown (PNEBD), whereas all zygotes spiked at this time in the presence of high extracellular Ca(2+)and dithiothreitol. Nucleated zygotic fragments also spiked before PNEBD whereas anucleated ones rarely did. Exit from G2 was required for this spiking to be observed in nucleated zygotes or fragments. Arrest in M-phase resulted in the appearance of a prolonged series of small amplitude spikes. It is concluded that the spiking at mitosis is cell cycle regulated and may differ qualitatively in its control from that at fertilization.