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.

位于母体中心粒的 Cep63-Cep152 复合体招募 Plk4 来启动中心粒生物发生。然而，该复合物如何靶向母体中心粒尚不清楚。在这项研究中，我们发现，在循环细胞和经历中心粒扩增的多纤毛细胞中，Cep57 及其旁系同源物 Cep57l1 与 Cep63 和 Cep152 共定位于母中心粒的近端。Cep57 和 Cep57l1 均与 Cep63 的中心体靶向区域结合。两种蛋白质（但不是其中任何一种）的耗尽会阻止 Cep63-Cep152 复合物加载到母体中心粒，从而防止中心粒复制。我们认为 Cep57 和 Cep57l1 功能冗余，以确保将 Cep63-Cep152 复合物招募到母中心粒以形成原中心粒。