A cytoplasmic cell cycle controls the activity of a K+ channel in pre-implantation mouse embryos
A cytoplasmic cell cycle controls the activity of a K+ channel in pre-implantation mouse embryos
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DOI：
10.1093/emboj/17.7.1952
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发表时间：
1998-04-01
期刊：
影响因子：
11.4
通讯作者：
Cook, DI
中科院分区：
文献类型：
--
作者：
Day, ML;Johnson, MH;Cook, DI
我们以前曾报道，在植入前小鼠胚胎的细胞周期中，240 pS K+通道的活性变化。在本研究中，我们表明：（i）通道活性的循环不阻止抑制蛋白质合成，因此不涉及细胞周期蛋白依赖性激酶1（cdk 1）-细胞周期蛋白B;和（ii）通道活性的循环继续在无核受精卵片段与有核片段中观察到的时间过程相似。我们进一步证明：（i）在中期停滞的单细胞胚胎中K+通道的持续激活需要维持活性cdk 1-细胞周期蛋白B复合物;和（ii）用阿非迪霉素的DNA合成抑制和由丝裂霉素C产生的DNA损伤都通过需要酪氨酸激酶激活的机制防止在S期开始时通道的下调。因此，这些细胞中的240 pS K+通道由先前未被怀疑的细胞质时钟控制，该细胞质时钟独立于众所周知的控制染色体细胞周期的时钟发挥作用，但可以与其相互作用。
We previously have reported that the activity of a 240 pS K+ channel varies during the cell cycle in preimplantation mouse embryos. In the present study, we show that: (i) the cycling of channel activity is not prevented by inhibiting protein synthesis and hence does not involve cyclin-dependent kinase 1 (cdk1)-cyclin B; and (ii) the cycling of channel activity continues in anucleate zygote fragments with a time course similar to that observed in nucleate fragments. We further demonstrate that: (i) persistent activation of the K+ channel in one-cell embryos arrested in metaphase requires the maintenance of an active cdk1-cyclin B complex; and (ii) both DNA synthesis inhibition with aphidicolin and DNA damage produced by mitomycin C prevent the down-regulation of the channel at the start of S phase by a mechanism that requires tyrosine kinase activation. Thus, the 240 pS K+ channel in these cells is controlled by a previously unsuspected cytoplasmic clock that functions independently of the well-known clock controlling the chromosomal cell cycle, but can interact with it.