期刊
CELL RESEARCH
卷 23, 期 11, 页码 1284-1295出版社
INST BIOCHEMISTRY & CELL BIOLOGY
DOI: 10.1038/cr.2013.127
关键词
cell cycle; FOR20; Plk1; S-phase; DNA replication
类别
资金
- Ministry of Science and Technology of China [2013CB945603, 2012CB945004, 2011CBA01001]
- National Natural Science Foundation of China [31071221, 31190063, 31125017]
- 111 Project [B13026]
- Natural Science Foundation of Zhejiang Province, China [Z2100247, Y2100106]
- Department of Science and Technology of Zhejiang Province [2009C03012-3, 2009F80005]
- Department of Health of Zhejiang Province [WKJ2006-2-014]
- Zhejiang Provincial Program for the Cultivation of High-level Innovative Health talents
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 Plk1 (polo-like kinase 1) to centrosomes, where FOR20 interacts with Plk1. Ablation of Plk1 also significantly induces S-phase defects, which are reversed by ectopic expression of Plk1, even a kinase-dead mutant, but not a mutant that fails to localize to centrosomes. Exogenous expression of centrosome-tethered Plk1, but not wild-type Plk1, overrides FOR20 depletion-induced S-phase defects independently of its kinase activity. Thus, these data indicate that recruitment of Plk1 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.
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