Polo-like kinase 3 is required for entry into S phase.
Polo-like kinase 3 is required for entry into S phase.
复制标题
进入 S 期需要 Polo 样激酶 3。
DOI：
10.1073/pnas.0610856104
复制
发表时间：
2007
影响因子：
11.1
通讯作者：
Erikson,RaymondL
中科院分区：
文献类型：
--
作者：
Zimmerman,WendyC;Erikson,RaymondL
Plk1在有丝分裂中表达和活跃，参与有丝分裂进入、纺锤杆组装、有丝分裂退出和细胞分裂[Donaldson m ., Tavares a ., Hagan m ., Nigg a ., Glover m ., 2001]。在哺乳动物中，还有两个不太为人所知的polo样激酶家族成员，Plk2和Plk3。plk3首先被鉴定并克隆为一个直接早期基因。在这里，我们报道Plk3定位于核仁并参与G1/S相变的调控。我们发现Plk3蛋白水平受细胞周期调控，在G1达到峰值。我们用慢病毒将Plk3干扰RNA传递到血清饥饿的细胞中，发现在血清刺激下，Plk3是cyclin E表达和进入S期所必需的。Plk3干扰rna诱导的Plk3缺失导致大部分异步增殖细胞进入静止状态。我们提出细胞周期中Plk3的要求在G1期得到满足，一旦细胞通过这一点，它们就能够完成细胞分裂，而在没有Plk3的情况下，它们无法重新进入细胞周期。其他数据表明，Plk3可能部分通过与磷酸酶Cdc25A相互作用调节进入S期，因为它的缺失也导致cyclin E表达的衰减。
The polo-like kinase, Plk1, which is expressed and active in mitosis, is involved in regulation of mitotic entry, spindle pole assembly, mitotic exit, and cytokinesis [Donaldson MM, Tavares AA, Hagan IM, Nigg EA, Glover DM (2001)J Cell Sci114:2357–2358]. In mammals, there are two other members of the polo-like kinase family that are less well understood, Plk2 and Plk3.Plk3first was identified and cloned as an immediate early gene. Here, we report Plk3 localizes to the nucleolus and is involved in regulation of the G1/S phase transition. We demonstrate that the level of Plk3 protein is cell cycle regulated, peaking in G1. We have delivered Plk3-interfering RNA with lentivirus to serum-starved cells and found that, upon serum stimulation, Plk3 is required for cyclin E expression and entry into S phase. Plk3-interfering RNA-induced Plk3 depletion resulted in a large fraction of asynchronously proliferating cells to become quiescent. We propose the Plk3 requirement in the cell cycle is fulfilled in G1, and that once cells pass this point, they are able to complete cell division, whereas in the absence of Plk3, they fail to reenter the cell cycle. Additional data suggest that Plk3 may regulate entry into S phase in part through interaction with the phosphatase Cdc25A, because its depletion also resulted in attenuation of cyclin E expression.