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首页> 外文期刊>Cell cycle >Chk1 is activated at the midblastula transition in Xenopus laevis embryos independently of DNA content and the cyclin E/Cdk2 developmental timer.
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Chk1 is activated at the midblastula transition in Xenopus laevis embryos independently of DNA content and the cyclin E/Cdk2 developmental timer.

机译：Chk1在非洲爪蟾胚胎的中胚层过渡期被激活，与DNA含量和细胞周期蛋白E / Cdk2发育计时器无关。

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摘要

Cell cycle checkpoints that are engaged in response to damaged and unreplicated DNA may serve additional, constitutive functions. In the developing Xenopus laevis embryo, the checkpoint kinase Chk1 is transiently activated at the midblastula transition (MBT), a period of extensive cell cycle remodeling including the acquisition of cell cycle checkpoints. The timing of many cell cycle remodeling events at the MBT, such as the lengthening of cell cycles, depends upon a critical nucleocytoplasmic (N/C) ratio. However, other events, including the degradation of maternal cyclin E, do not depend upon the N/C ratio, and are regulated by an autonomous developmental timer. To better understand what regulates Chk1 activation at the MBT, embryos were treated with aphidicolin, at different developmental times and for different lengths of time, to reduce the DNA content at the MBT. Chk1 was activated at the MBT in these embryos establishing that Chk1 activation occurs independently of the N/C ratio. Cdc25A is normally phosphorylated by Chk1 at the MBT and then degraded. The degradation of Cdc25A demonstrated partial dependence on DNA content, suggesting that factors other than Chk1 regulate its degradation. When the cyclin E developmental timer was disrupted with the Cdk2 inhibitor delta34-Xic1, Chk1 was still activated at the MBT, indicating that activation of Chk1 at the MBT was not directly linked to the cyclin E timer. Conversely, unreplicated or damaged DNA, delayed the degradation of cyclin E at the MBT, indicating that the cyclin E/Cdk2 timer is sensitive to engagement of cell cycle checkpoints.
机译：响应受损和未复制的DNA而参与的细胞周期检查点可能具有额外的组成功能。在发育中的非洲爪蟾胚胎中，检查点激酶Chk1在中胚层过渡期（MBT）短暂激活，MBT是一段广泛的细胞周期重塑时期，包括获取细胞周期检查点。 MBT上许多细胞周期重塑事件的时间（例如细胞周期的延长）取决于关键的核质（N / C）比。但是，其他事件，包括母体细胞周期蛋白E的降解，并不取决于N / C比率，而是由自主发育定时器来调节。为了更好地了解什么在MBT上调节Chk1的活化，在不同的发育时间和不同的时间长度，用蚜虫碱处理了胚胎，以减少MBT上的DNA含量。这些胚胎在MBT处激活了Chk1，从而确定了Chk1的激活独立于N / C比而发生。 Cdc25A通常在MBT处被Chk1磷酸化，然后降解。 Cdc25A的降解表现出对DNA含量的部分依赖性，这表明除Chk1以外的其他因素也可调节其降解。当Cdk2抑制剂delta34-Xic1破坏了细胞周期蛋白E的发育定时器时，Chk1在MBT上仍被激活，这表明在MBT上Chk1的激活并不与细胞周期蛋白E定时器直接相关。相反，未复制或损坏的DNA延迟了MBT上细胞周期蛋白E的降解，这表明细胞周期蛋白E / Cdk2计时器对细胞周期检查点的参与很敏感。

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