Full-term mouse development by abolishing Zn2+-dependent metaphase II arrest without Ca2+ release

T Suzuki, N Yoshida, E Suzuki, E Okuda, Anthony C F Perry

Research output: Contribution to journalArticle

55 Citations (Scopus)

Abstract

In vertebrates, a rise in intracellular free Ca2+ (Ca-i(2+)) levels during fertilization initiates second metaphase (mII) exit and the developmental programme. The Ca2+ rise has long been considered to be crucial for development, but verifying this contribution would benefit from defining its role during fertilization. Here, we delineate the role of Ca2+ release during mII exit in wild-type mouse eggs and show that it is dispensable for full-term development. Exit from mII can be induced by Zn2+-specific sequestration without Ca2+ release, eliciting Cyclin B degradation in a manner dependent upon the proteasome pathway and intact microtubules, but not accompanied by degradation of the meiotic regulator Emi2. Parthenogenotes generated by Zn2+ sequestration developed in vitro with normal expression of Ca2+-sensitive genes. Meiotic exit induced by either Ca2+ oscillations or a single Ca2+ rise in oocytes containing a signaling-deficient sperm resulted in comparable developmental rates. In the absence of Ca2+ release, full-term development occurred similar to 50% less efficiently, but at readily detectable rates, with the birth of 27 offspring. These results show in intact mouse oocytes that Zn2+ is essential for mII arrest and suggest that triggering meiotic exit is the sole indispensable developmental role of Ca2+ signaling in mammalian fertilization.
Original languageEnglish
Pages (from-to)2659-2669
Number of pages11
JournalDevelopment
Volume137
Issue number16
Early online date29 Jun 2010
DOIs
Publication statusPublished - 15 Aug 2010

Keywords

  • mouse
  • metaphase II exit
  • Zn2+
  • Ca2+

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