Lee Seung Baek, Kim Jung Jin, Nam Hyun-Ja, Gao Bowen, Yin Ping, Qin Bo, Yi Sang-Yeop, Ham Hyoungjun, Evans Debra, Kim Sun-Hyun, Zhang Jun, Deng Min, Liu Tongzheng, Zhang Haoxing, Billadeau Daniel D, Wang Liewei, Giaime Emilie, Shen Jie, Pang Yuan-Ping, Jen Jin, van Deursen Jan M, Lou Zhenkun
Division of Oncology Research, Mayo Clinic, Rochester, MN 55905, USA.
Department of Pediatric and Adolescent Medicine, Mayo Clinic, Rochester, MN 55905, USA.
Mol Cell. 2015 Oct 1;60(1):21-34. doi: 10.1016/j.molcel.2015.08.011. Epub 2015 Sep 17.
Mutations in the E3 ubiquitin ligase Parkin have been linked to familial Parkinson's disease. Parkin has also been implicated in mitosis through mechanisms that are unclear. Here we show that Parkin interacts with anaphase promoting complex/cyclosome (APC/C) coactivators Cdc20 and Cdh1 to mediate the degradation of several key mitotic regulators independent of APC/C. We demonstrate that ordered progression through mitosis is orchestrated by two distinct E3 ligases through the shared use of Cdc20 and Cdh1. Furthermore, Parkin is phosphorylated and activated by polo-like kinase 1 (Plk1) during mitosis. Parkin deficiency results in overexpression of its substrates, mitotic defects, genomic instability, and tumorigenesis. These results suggest that the Parkin-Cdc20/Cdh1 complex is an important regulator of mitosis.
E3泛素连接酶帕金(Parkin)的突变与家族性帕金森病有关。帕金还通过尚不清楚的机制参与有丝分裂。在此我们表明,帕金与后期促进复合物/细胞周期体(APC/C)共激活因子Cdc20和Cdh1相互作用,以介导几种关键有丝分裂调节因子的降解,且不依赖于APC/C。我们证明,有丝分裂的有序进程是由两种不同的E3连接酶通过共同利用Cdc20和Cdh1精心安排的。此外,在有丝分裂期间,帕金被polo样激酶1(Plk1)磷酸化并激活。帕金缺乏会导致其底物的过度表达、有丝分裂缺陷、基因组不稳定和肿瘤发生。这些结果表明,帕金-Cdc20/Cdh1复合物是有丝分裂的重要调节因子。