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Requirement of the Cep57-Cep63 Interaction for Proper Cep152 Recruitment and Centriole Duplication.
Molecular and Cellular Biology ( IF 5.3 ) Pub Date : 2020-04-28 , DOI: 10.1128/mcb.00535-19
Zhuang Wei 1 , Tae-Sung Kim 1 , Jong Il Ahn 1 , Lingjun Meng 1 , Yaozong Chen 1 , Eun Kyoung Ryu 2 , Bonsu Ku 3 , Ming Zhou 4 , Seung Jun Kim 3 , Jeong Kyu Bang 2 , Jan M van Deursen 5, 6 , Jung-Eun Park 1 , Kyung S Lee 7
Affiliation  

Cep57 has been characterized as a component of a pericentriolar complex containing Cep63 and Cep152. Interestingly, Cep63 and Cep152 self-assemble into a pericentriolar cylindrical architecture, and this event is critical for the orderly recruitment of Plk4, a key regulator of centriole duplication. However, the way in which Cep57 interacts with the Cep63-Cep152 complex and contributes to the structure and function of Cep63-Cep152 self-assembly remains unknown. We demonstrate that Cep57 interacts with Cep63 through N-terminal motifs and associates with Cep152 via Cep63. Three-dimensional structured illumination microscopy (3D-SIM) analyses suggested that the Cep57-Cep63-Cep152 complex is concentrically arranged around a centriole in a Cep57-in and Cep152-out manner. Cep57 mutant cells defective in Cep63 binding exhibited improper Cep63 and Cep152 localization and impaired Sas6 recruitment for procentriole assembly, proving the significance of the Cep57-Cep63 interaction. Intriguingly, Cep63 fused to a microtubule (MT)-binding domain of Cep57 functioned in concert with Cep152 to assemble around stabilized MTs in vitro Thus, Cep57 plays a key role in architecting the Cep63-Cep152 assembly around centriolar MTs and promoting centriole biogenesis. This study may offer a platform to investigate how the organization and function of the pericentriolar architecture are altered by disease-associated mutations found in the Cep57-Cep63-Cep152 complex.

中文翻译:

Cep57-Cep63交互对正确Cep152招聘和中心复制的要求。

Cep57已被表征为包含Cep63和Cep152的中央小周复合体的组成部分。有趣的是,Cep63和Cep152自组装为中心小周圆柱形结构,此事件对于有序募集中心粒重复的关键调节子Plk4至关重要。但是,Cep57与Cep63-Cep152复合体相互作用并促进Cep63-Cep152自组装的结构和功能的方式仍然未知。我们证明,Cep57通过N端基序与Cep63相互作用,并通过Cep63与Cep152相关联。三维结构化照明显微镜(3D-SIM)分析表明,Cep57-Cep63-Cep152复合物以Cep57-in和Cep152-out的方式同心地围绕着一个心轴排列。Cep63结合缺陷的Cep57突变细胞表现出不正确的Cep63和Cep152定位,以及原中心组装的Sas6募集受损,证明了Cep57-Cep63相互作用的重要性。有趣的是,与Cep57的微管(MT)结合域融合的Cep63与Cep152协同起作用,在体外稳定的MT周围组装。因此,Cep57在构建围绕着中心粒MT的Cep63-Cep152装配并促进中心粒生物发生中起着关键作用。这项研究可能提供一个平台,以研究在Cep57-Cep63-Cep152复合物中发现的与疾病相关的突变如何改变中心小肠周围结构的组织和功能。融合到Cep57的微管(MT)结合结构域的Cep63与Cep152协同起作用,在体外围绕稳定的MT组装。因此,Cep57在构建围绕着中心粒MT的Cep63-Cep152组装并促进中心粒生物发生方面起着关键作用。这项研究可能提供一个平台,以研究在Cep57-Cep63-Cep152复合物中发现的与疾病相关的突变如何改变中心小肠周围结构的组织和功能。融合到Cep57的微管(MT)结合结构域的Cep63与Cep152协同起作用,在体外围绕稳定的MT组装。因此,Cep57在构建围绕着中心粒MT的Cep63-Cep152组装并促进中心粒生物发生方面起着关键作用。这项研究可能提供一个平台,以研究在Cep57-Cep63-Cep152复合物中发现的与疾病相关的突变如何改变中心小肠周围结构的组织和功能。
更新日期:2020-04-28
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