State Key Laboratory of Cell Biology, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences, Shanghai 200031, China.
University of Chinese Academy of Sciences, Beijing 100049, China.
J Cell Sci. 2020 Jul 3;133(13):jcs241836. doi: 10.1242/jcs.241836.
The Cep63-Cep152 complex located at the mother centriole recruits Plk4 to initiate centriole biogenesis. How the complex is targeted to mother centrioles, however, is unclear. In this study, we show that Cep57 and its paralog, Cep57l1, colocalize with Cep63 and Cep152 at the proximal end of mother centrioles in both cycling cells and multiciliated cells undergoing centriole amplification. Both Cep57 and Cep57l1 bind to the centrosomal targeting region of Cep63. The depletion of both proteins, but not either one, blocks loading of the Cep63-Cep152 complex to mother centrioles and consequently prevents centriole duplication. We propose that Cep57 and Cep57l1 function redundantly to ensure recruitment of the Cep63-Cep152 complex to the mother centrioles for procentriole formation.
位于母中心体的 Cep63-Cep152 复合物招募 Plk4 起始中心体发生。然而，该复合物如何靶向母中心体尚不清楚。在本研究中，我们发现 Cep57 及其同源物 Cep57l1 在有丝分裂细胞和进行中心体扩增的多纤毛细胞的母中心体的近端与 Cep63 和 Cep152 共定位。Cep57 和 Cep57l1 都与 Cep63 的中心体靶向区域结合。两种蛋白的耗竭（而非单独一种）阻断了 Cep63-Cep152 复合物加载到母中心体上，从而阻止了中心体复制。我们提出 Cep57 和 Cep57l1 冗余地发挥作用，以确保 Cep63-Cep152 复合物招募到母中心体，用于形成前中心体。
