We are delighted to publish Part 2 of our Special Issue on cell cycle control. Here, we present four reviews that, together with Part 1, give a comprehensive overview of our current understanding of the cell cycle, as well as the methods employed to study it, the roles of cell cycle proteins beyond orchestrating cell division, and some of the key outstanding questions. Part 1 provided an overview of the common principles governing the transitions between the cell cycle phases [1], the role of metabolism in quiescence–proliferation transitions [2] and the relationship between the speed of the cell cycle and cell fate [3]. In addition, Part 1 covered how cells prepare for DNA replication during G1 and how this impacts proper DNA replication in S-phase [4], how cells control entry into mitosis [5] and, once in mitosis, how they achieve proper chromosome alignment and equal segregation of chromosomes into two daughter cells [6], and how mitotic exit is controlled to ensure appropriate temporal and spatial organisation [7]. A comparison between the function of CDKs in mitosis and meiosis concluded Part 1 [8]. Part 2 begins with a review from Silvia Santos’ Lab that covers how embryonic cell cycles remodel in order to give rise to somatic cell cycles, including the, often forgotten, differences between human and mouse embryonic stem cells [9]. Adaptation of embryonic cell cycles to somatic cell cycles requires extensive changes in the regulation of cyclins, CDKs and the anaphasepromoting complex/cyclosome, as well as the introduction of cell cycle checkpoints. A notable example of the checkpoints that are introduced en route to somatic cell cycles is the restriction point. The restriction point is defined as the point in the cell cycle beyond which cells no longer require input from mitogens to complete cell division. In a review from our laboratory, we discuss and analyse recent data to understand the control of the restriction point in determining proliferation–quiescence decisions in cells [10]. The restriction point was originally defined over 40 years ago, yet its position within the cell cycle and the molecular basis for this decision are still active topics of investigation. From proliferation–quiescence decisions, we then move onto proliferation–differentiation decisions, in a review from the Kimata and Aradhya laboratories [11]. Much has been written in this review series about the roles of cyclin:CDK complexes in driving the cell cycle. However, here the focus is on the cell cycle-independent roles of cyclins, CDKs and their inhibitors, in particular in their contributions to cell differentiation. It is critical to remember these non-cell cycle functions, particularly when analysing the phenotypes of mice where the function of these proteins has been disrupted. Finally, Anna Eastman and Shangqin Guo have provided a second review for this series, and this one focussed on the methods available to study and probe the cell cycle [12]. We imagine that this will be of particular interest to researchers new to the field but also serves as a very useful reminder to experts as to the strengths and weaknesses of our assays. We anticipate that readers new to the cell cycle field and also aficionados of cell cycle control will enjoy this special issue. Hopefully, these reviews, written by leaders in cell cycle research, will spark new questions and ideas to keep expanding our understanding of the phenomenal and beautiful process that is cell division.

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社论

我们很高兴发布有关细胞周期控制的特刊的第 2 部分。在这里，我们提出了四篇评论，连同第 1 部分，全面概述了我们目前对细胞周期的理解，以及用于研究它的方法，细胞周期蛋白在协调细胞分裂之外的作用，以及一些关键悬而未决的问题。第 1 部分概述了控制细胞周期阶段之间转换的通用原则 [1]、代谢在静止-增殖转换中的作用 [2] 以及细胞周期速度与细胞命运之间的关系 [3]。此外，第 1 部分涵盖了细胞如何在 G1 期间为 DNA 复制做准备以及这如何影响 S 期的正确 DNA 复制 [4]、细胞如何控制进入有丝分裂 [5] 以及一旦进入有丝分裂，它们如何实现正确的染色体排列和将染色体均等分离成两个子细胞 [6]，以及如何控制有丝分裂退出以确保适当的时间和空间组织 [7]。CDKs 在有丝分裂和减数分裂中的功能比较在第 1 部分得出结论 [8]。第 2 部分以 Silvia Santos 实验室的综述开始，介绍胚胎细胞周期如何重塑以产生体细胞周期，包括经常被遗忘的人和小鼠胚胎干细胞之间的差异 [9]。胚胎细胞周期对体细胞周期的适应需要对细胞周期蛋白、CDK 和后期促进复合物/细胞周期体的调节进行广泛的改变，以及细胞周期检查点的引入。在进入体细胞周期的过程中引入的检查点的一个显着例子是限制点。限制点被定义为细胞周期中的点，超过该点细胞不再需要有丝分裂原的输入来完成细胞分裂。在我们实验室的一篇综述中，我们讨论和分析了最近的数据，以了解在决定细胞增殖 - 静止决策时限制点的控制 [10]。限制点最初是在 40 多年前定义的，但它在细胞周期中的位置和这一决定的分子基础仍然是研究的热点。在 Kimata 和 Aradhya 实验室的综述中，我们从增殖-静止决策转向增殖-分化决策[11]。本系列评论中已经写了很多关于细胞周期蛋白：CDK 复合物在驱动细胞周期中的作用的文章。然而，这里的重点是细胞周期蛋白、CDK 及其抑制剂的细胞周期独立作用，特别是它们对细胞分化的贡献。记住这些非细胞周期功能至关重要，特别是在分析这些蛋白质功能被破坏的小鼠表型时。最后，安娜·伊士曼 (Anna Eastman) 和郭尚琴 (Shangqin Guo) 为本系列提供了第二篇评论，这篇评论侧重于研究和探测细胞周期的可用方法 [12]。我们认为这对刚进入该领域的研究人员会特别感兴趣，但也可以作为一个非常有用的提示，提醒专家我们分析的优势和劣势。我们预计细胞周期领域的新读者以及细胞周期控制的爱好者都会喜欢这期特刊。希望这些由细胞周期研究领域的领导者撰写的评论将引发新的问题和想法，以不断扩大我们对细胞分裂这一惊人而美丽的过程的理解。