Maintenance of metaphase in colcemid-treated mouse eggs by distinct calcium- and 6-dimethylaminopurine (6-DMAP)-sensitive mechanisms.
Maintenance of metaphase in colcemid-treated mouse eggs by distinct calcium- and 6-dimethylaminopurine (6-DMAP)-sensitive mechanisms.
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DOI：
10.1006/dbio.1995.1027
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发表时间：
1995
影响因子：
2.7
通讯作者：
R. Moses;D. Kline;Y. Masui
中科院分区：
文献类型：
--
作者：
R. Moses;D. Kline;Y. Masui
在小鼠卵中，减数分裂中期II的停滞通过受精诱导的细胞内钙的增加而释放。当用微管抑制剂秋水仙胺处理的卵子受精或暴露于钙离子载体A23187时，会发生正常的钙增加，但卵子仍处于中期。然而，当秋水仙胺处理的卵子受精或A23187处理，然后暴露于蛋白激酶抑制剂6-二甲基氨基嘌呤（6-DMAP），他们进入间期。虽然秋水仙胺处理的卵需要钙信号和暴露于6-DMAP，但秋水仙胺处理的胚胎细胞通过6-DMAP处理而不是暴露于A23187而从中期释放。这些结果表明，两种不同的机制维持中期：一个是钙敏感的机制，涉及细胞生长抑制因子，通常维持中期II逮捕鸡蛋;另一种机制，这可能需要6-DMAP敏感激酶的活性，维持中期在没有纺锤体组装在有丝分裂细胞和鸡蛋。
In mouse eggs, the arrest at meiotic metaphase II is released by the fertilization-induced increase in intracellular calcium. When eggs treated with the microtubule inhibitor colcemid are fertilized or exposed to the calcium ionophore A23187, normal calcium increases occur, but the eggs remain at metaphase. However, when colcemid-treated eggs are fertilized or A23187-treated and then exposed to the protein kinase inhibitor 6-dimethylaminopurine (6-DMAP), they enter interphase. Although colcemid-treated eggs require a calcium signal and exposure to 6-DMAP, colcemid-treated embryonic cells are released from metaphase by treatment with 6-DMAP, but not by exposure to A23187. These results suggest that two distinct mechanisms maintain metaphase: one is the calcium-sensitive mechanism involving cytostatic factor, which normally maintains metaphase II arrest in eggs; the other mechanism, which may require the activity of 6-DMAP-sensitive kinases, maintains metaphase in the absence of spindle assembly in both mitotic cells and eggs.