Mik1 levels accumulate in S phase and may mediate an intrinsic link between S phase and mitosis
Mik1 levels accumulate in S phase and may mediate an intrinsic link between S phase and mitosis
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DOI：
10.1073/pnas.97.6.2579
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发表时间：
2000-03-14
影响因子：
11.1
通讯作者：
Carr, AM
中科院分区：
文献类型：
--
作者：
Christensen, PU;Bentley, NJ;Carr, AM
在细胞周期进程中维持秩序存在两种范式：内在控制，通过细胞周期的一部分直接影响执行另一部分的能力；检查点控制，外部途径对异常结构的响应施加秩序。通过对有丝分裂抑制剂Mik1的研究，我们已经发现了未受干扰的S期与有丝分裂之间内在联系的证据，我们提出了一个模型，在这个模型中，S期Mik1蛋白的产生和稳定可以产生S/M连锁。在未受干扰的S期，Mik1的产生独立于Rad3-和cds1依赖的检查点控制。在S期紊乱的情况下，需要Rad3-Cds1检查点控制来维持高水平的Mik1，这可能间接通过延长Mik1稳定的S期来实现。此外，我们发现Mik1蛋白可以以chk1依赖的方式适度诱导辐照G(2)细胞。
Two paradigms exist for maintaining order during cell-cycle progression: intrinsic controls, where passage through one part of the cell cycle directly affects the ability to execute another, and checkpoint controls, where external pathways impose order in response to aberrant structures. By studying the mitotic inhibitor Mik1, we have identified evidence for an intrinsic link between unperturbed S phase and mitosis, We propose a model in which S/M linkage can be generated by the production and stabilization of Mik1 protein during S phase. The production of Mik1 during unperturbed S phase is independent of the Rad3- and Cds1-dependent checkpoint controls. In response to perturbed S phase, Rad3-Cds1 checkpoint controls are required to maintain high levels of Mik1, probably indirectly by extending the S phase period, where Mik1 is stable. In addition, we find that Mik1 protein can be moderately induced in response to irradiation of G(2) cells in a Chk1-dependent manner.