Centrosomal protein FOR20 is essential for S-phase progression by recruiting Plkl to centrosomes  

作　　者：Minhong Shen Yuqi Cai YuehongYang Xiaoyi Yan Xiaoqi Liu Tianhua Zhou 

机构地区：[1]Department of Cell Biology and Program in Molecular Cell Biology, Zhejiang University School of Medicine, 866 Yuhangtang Road, Hangzhou, Zhejiang 310058, China [2]Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, Hangzhou, Zhejiang 310003, China [3]Department of Biochemistry, Purdue University, West Lafayette, IN 47907, USA

出　　处：《Cell Research》2013年第11期1284-1295,共12页细胞研究（英文版）

摘　　要：Centrosomes are required for efficient cell cycle progression mainly by orchestrating microtubule dynamics and facilitating G1/S and G2/M transitions. However, the role of centrosomes in S-phase progression is largely unknown. Here, we report that depletion of FOR20 （FOP-related protein of 20 kDa）, a conserved centrosomal protein, inhibits S-phase progression and prevents targeting of Plkl （polo-like kinase 1） to centrosomes, where FOR20 interacts with Plkl. Ablation of Plkl also significantly induces S-phase defects, which are reversed by ectopic expression of Plkl, even a kinase-dead mutant, but not a mutant that fails to localize to centrosomes. Exogenous expression of centro- some-tethered Plkl, but not wild-type Plkl, overrides FOR20 depletion-induced S-phase defects independently of its kinase activity. Thus, these data indicate that recruitment of Plkl to centrosomes by FOR20 may act as a signal to license efficient progression of S-phase. This represents a hitherto uncharacterized role of centrosomes in cell cycle regulation.Centrosomes are required for efficient cell cycle progression mainly by orchestrating microtubule dynamics and facilitating G1/S and G2/M transitions. However, the role of centrosomes in S-phase progression is largely unknown. Here, we report that depletion of FOR20 （FOP-related protein of 20 kDa）, a conserved centrosomal protein, inhibits S-phase progression and prevents targeting of Plkl （polo-like kinase 1） to centrosomes, where FOR20 interacts with Plkl. Ablation of Plkl also significantly induces S-phase defects, which are reversed by ectopic expression of Plkl, even a kinase-dead mutant, but not a mutant that fails to localize to centrosomes. Exogenous expression of centro- some-tethered Plkl, but not wild-type Plkl, overrides FOR20 depletion-induced S-phase defects independently of its kinase activity. Thus, these data indicate that recruitment of Plkl to centrosomes by FOR20 may act as a signal to license efficient progression of S-phase. This represents a hitherto uncharacterized role of centrosomes in cell cycle regulation.

关 键 词：cell cycle FOR20 Plkl S-PHASE DNA replication 

分 类 号：Q492.4[生物学—生理学] S865.13[农业科学—野生动物驯养]