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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 language | English |
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Pages (from-to) | 2659-2669 |
Number of pages | 11 |
Journal | Development |
Volume | 137 |
Issue number | 16 |
Early online date | 29 Jun 2010 |
DOIs | |
Publication status | Published - 15 Aug 2010 |
Keywords
- mouse
- metaphase II exit
- Zn2+
- Ca2+
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Dive into the research topics of 'Full-term mouse development by abolishing Zn2+-dependent metaphase II arrest without Ca2+ release'. Together they form a unique fingerprint.Projects
- 1 Finished
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Tony Perry - Transgenic Models of Mammalian Meiotic Exit
Perry, T. (PI)
1/04/10 → 31/03/14
Project: EU Commission