Checkpoint adaptation and recovery - Back with polo after the break

被引:39
作者
van Vugt, MATM [1 ]
Medema, RH [1 ]
机构
[1] Antoni Van Leeuwenhoek Hosp, Netherlands Canc Inst, Div Mol Biol, NL-1066 CX Amsterdam, Netherlands
关键词
cell cycle; genetic instability; cdc20 genotoxic stress;
D O I
10.4161/cc.3.11.1248
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
S. cerevisiae cells that are unable to repair a double strand break ultimately escape the DNA damage checkpoint arrest and enter mitosis. This process called 'adaptation' depends on functional Cdc5, a Polo-like kinase, and was long thought to be limited to single-cell organisms. However, the recent finding that Xenopus extracts can adapt to a long-lasting stall in DNA replication indicates that checkpoint adaptation does also occur in multicellular organisms. Interestingly, the Xenopus Polo-like kinase (Plx1) plays an important role in this adaptation. To add to this, data from our laboratory have shown that the human Polo-like kinase (Plk1) is also required for cell cycle reentry following a DNA damage-induced arrest. But here, Plk1 was shown to be required for bona-fide checkpoint recovery, rather than adaptation. That is, Plk1 is required to restart the cell cycle once all of the damage is repaired and checkpoint signaling is turned off. While the target of Plx1 during adaptation is a component of the checkpoint machinery ( Claspin), the target of Plk1 during recovery turns out to be a mitotic regulator (Wee1). Here, we discuss some of the remarkable similarities and subtle differences in the molecular mechanisms that control checkpoint adaptation and recovery, and the role of Polo-like kinases therein.
引用
收藏
页码:1383 / 1386
页数:4
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