Getting to S: CDK functions and targets on the path to cell-cycle commitment.
Getting to S: CDK functions and targets on the path to cell-cycle commitment.
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DOI：
10.12688/f1000research.9463.1
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发表时间：
2016
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影响因子：
--
通讯作者：
Fisher RP
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文献类型：
--
作者：
Fisher RP
真核细胞如何以及何时做出不可撤销的分裂承诺仍然是细胞周期领域的中心问题。在酵母和哺乳动物细胞中的平行研究似乎表明，类似的控制机制在G1期的开始或限制（R）点，分别整合营养和发育信号，并决定不同的细胞命运：细胞周期停滞或退出与不可逆的承诺一轮分裂。最近的研究揭示了酵母和哺乳动物细胞中这一决策过程的分子机制，但也对多细胞生物中细胞周期承诺的性质和时间产生了怀疑。这些研究表明，在某些生长条件下，有丝分裂原传感的时间窗口扩大，照亮了意想不到的障碍和退出坡道的道路上，以完整的细胞周期的承诺，并提出了新的问题，驱动G1期进展和S期进入的细胞周期蛋白依赖性激酶（CDKs）的功能。
How and when eukaryotic cells make the irrevocable commitment to divide remain central questions in the cell-cycle field. Parallel studies in yeast and mammalian cells seemed to suggest analogous control mechanisms operating during the G1 phase—at Start or the restriction (R) point, respectively—to integrate nutritional and developmental signals and decide between distinct cell fates: cell-cycle arrest or exit versus irreversible commitment to a round of division. Recent work has revealed molecular mechanisms underlying this decision-making process in both yeast and mammalian cells but also cast doubt on the nature and timing of cell-cycle commitment in multicellular organisms. These studies suggest an expanded temporal window of mitogen sensing under certain growth conditions, illuminate unexpected obstacles and exit ramps on the path to full cell-cycle commitment, and raise new questions regarding the functions of cyclin-dependent kinases (CDKs) that drive G1 progression and S-phase entry.