Full-term mouse development by abolishing Zn2+-dependent metaphase II arrest without Ca2+ release
Suzuki, T., Yoshida, N., Suzuki, E., Okuda, E. and Perry, A. C. F., 2010. Full-term mouse development by abolishing Zn2+-dependent metaphase II arrest without Ca2+ release. Development, 137 (16), pp. 2659-2669.
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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.
|Creators||Suzuki, T., Yoshida, N., Suzuki, E., Okuda, E. and Perry, A. C. F.|
|Uncontrolled Keywords||mouse, metaphase ii exit, zn2+, ca2+|
|Departments||Faculty of Science > Biology & Biochemistry|
|Research Centres||Centre for Regenerative Medicine|
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