The proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit.
The proliferation-quiescence decision is controlled by a bifurcation in CDK2 activity at mitotic exit.
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DOI：
10.1016/j.cell.2013.08.062
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发表时间：
2013-10-10
期刊：
影响因子：
64.5
通讯作者：
Meyer T
中科院分区：
文献类型：
--
作者：
Spencer SL;Cappell SD;Tsai FC;Overton KW;Wang CL;Meyer T
后生动物的组织稳态是通过细胞在静止和增殖之间的转变来调节的。群体增殖的标志是细胞周期的进展，这是由细胞周期蛋白依赖性激酶 (CDK) 活性驱动的。在这里，我们引入了一种用于检测 CDK2 活性的活细胞传感器，并意外地发现增殖细胞在退出有丝分裂时分成两个群体。许多细胞通过从中间水平建立 CDK2 活性来立即进入下一个细胞周期，而其他细胞则缺乏 CDK2 活性并进入短暂的静止状态。这种分叉直接由 CDK 抑制剂 p21 控制，并在前一个细胞周期结束时的限制窗口期间由有丝分裂原调节。因此，细胞在有丝分裂结束时决定是通过立即增强 CDK2 活性来开始下一个细胞周期，还是通过抑制 CDK2 活性进入短暂的 G0 样状态。
Tissue homeostasis in metazoans is regulated by transitions of cells between quiescence and proliferation. The hallmark of proliferating populations is progression through the cell cycle, which is driven by cyclin-dependent kinase (CDK) activity. Here, we introduce a live-cell sensor for CDK2 activity and unexpectedly found that proliferating cells bifurcate into two populations as they exit mitosis. Many cells immediately commit to the next cell cycle by building up CDK2 activity from an intermediate level, while other cells lack CDK2 activity and enter a transient state of quiescence. This bifurcation is directly controlled by the CDK inhibitor p21 and is regulated by mitogens during a restriction window at the end of the previous cell cycle. Thus, cells decide at the end of mitosis to either start the next cell cycle by immediately building up CDK2 activity or to enter a transient G0-like state by suppressing CDK2 activity.
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影响因子：
4.8
作者：
Debnath, J;Muthuswamy, SK;Brugge, JS
通讯作者：
Brugge, JS
影响因子：
56.9
作者：
KOFF, A;GIORDANO, A;ROBERTS, JM
通讯作者：
ROBERTS, JM
影响因子：
64.5
作者：
Sakaue-Sawano, Asako;Kurokawa, Hiroshi;Miyawaki, Atsushi
通讯作者：
Miyawaki, Atsushi
影响因子：
5.3
作者：
Lanni, JS;Jacks, T
通讯作者：
Jacks, T
DOI：
10.4161/cc.8.7.8042
发表时间：
2009-04-01
期刊：
Cell cycle (Georgetown, Tex.)
影响因子：
--
作者：
Hahn AT;Jones JT;Meyer T
通讯作者：
Meyer T