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Rise of intracellular Ca2+ level causes the decrease of cyclin B1 and Mos in the newt eggs at fertilization
S Yamamoto1, M Yamashita, Y Iwao
1Department of Biological Science, Faculty of Science, Yamaguchi University, Japan.
Molecular Reproduction and Development
|June 16, 1999
Summary
Fertilization triggers a calcium ion increase in newt eggs, initiating cell cycle resumption. This calcium surge degrades cyclin B1 and Mos, preventing new synthesis and enabling meiosis completion.
Area of Science:
- Developmental Biology
- Cell Cycle Regulation
- Calcium Signaling
Background:
- Newt eggs (Cynops pyrrhogaster) arrest at the second meiotic metaphase with high M-phase promoting factor (MPF) activity.
- Fertilization triggers the resumption of the cell cycle and emission of the second polar body.
Purpose of the Study:
- To investigate the role of intracellular calcium ([Ca2+]i) in the resumption of meiosis in newt eggs after fertilization.
- To elucidate the molecular mechanisms underlying cell cycle reinitiation.
Main Methods:
- Monitoring intracellular calcium changes using aequorin.
- Inhibiting calcium signaling with 1,2-Bis (2 aminophenoxy) ethane-N,N,N',N',-tetraacetic acid (BAPTA).
- Analyzing protein levels (cyclin B1, Mos) via Western blot and assessing chymotryptic activity.
Main Results:
- Fertilization induced early and late increases in [Ca2+]i.
- BAPTA injection blocked cell cycle reinitiation.
- Cyclin B1 and Mos proteins degraded post-fertilization; Ca2+-ionophore treatment mimicked this effect.
- Cycloheximide treatment decreased cyclin B1 and Mos without altering [Ca2+]i.
Conclusions:
- Increased intracellular calcium ([Ca2+]i) at fertilization induces meiotic resumption in newt eggs.
- Calcium signaling leads to the degradation of cyclin B1 and Mos by inhibiting their synthesis.
- This calcium-dependent degradation is crucial for completing meiosis.