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Cep169,一种新型的微管正端追踪中心体蛋白,与CDK5RAP2结合并调节微管稳定性。

Cep169, a Novel Microtubule Plus-End-Tracking Centrosomal Protein, Binds to CDK5RAP2 and Regulates Microtubule Stability.

作者信息

Mori Yusuke, Inoue Yoko, Tanaka Sayori, Doda Satoka, Yamanaka Shota, Fukuchi Hiroki, Terada Yasuhiko

机构信息

Department of Chemistry and Biochemistry, School of Advanced Science and Engineering, Waseda University, 3-4-1 Ohkubo, Tokyo 169-8555, Japan.

出版信息

PLoS One. 2015 Oct 20;10(10):e0140968. doi: 10.1371/journal.pone.0140968. eCollection 2015.

Abstract

The centrosomal protein, CDK5RAP2, is a microcephaly protein that regulates centrosomal maturation by recruitment of a γ-tubulin ring complex (γ-TuRC) onto centrosomes. In this report, we identified a novel human centrosomal protein, Cep169, as a binding partner of CDK5RAP2, a member of microtubule plus-end-tracking proteins (+TIPs). Cep169 interacts directly with CDK5RAP2 through CM1, an evolutionarily conserved domain, and colocalizes at the pericentriolar matrix (PCM) around centrioles with CDK5RAP2. In addition, Cep169 interacts with EB1 through SxIP-motif responsible for EB1 binding, and colocalizes with CDK5RAP2 at the microtubule plus-end. EB1-binding-deficient Cep169 abolishes EB1 interaction and microtubule plus-end attachment, indicating Cep169 as a novel member of +TIPs. We further show that ectopic expression of either Cep169 or CDK5RAP2 induces microtubule bundling and acetylation in U2OS cells, and depletion of Cep169 induces microtubule depolymerization in HeLa cells, although Cep169 is not required for assembly of γ-tubulin onto centrosome by CDK5RAP2. These results show that Cep169 targets microtubule tips and regulates stability of microtubules with CDK5RAP2.

摘要

中心体蛋白CDK5RAP2是一种小头畸形蛋白,它通过将γ-微管蛋白环复合物(γ-TuRC)募集到中心体上来调节中心体成熟。在本报告中,我们鉴定出一种新型人类中心体蛋白Cep169,它是CDK5RAP2的结合伴侣,CDK5RAP2是微管正端追踪蛋白(+TIPs)的成员之一。Cep169通过CM1(一个进化上保守的结构域)直接与CDK5RAP2相互作用,并与CDK5RAP2共定位于中心粒周围的中心粒外周基质(PCM)。此外,Cep169通过负责与EB1结合的SxIP基序与EB1相互作用,并与CDK5RAP2在微管正端共定位。缺乏EB1结合能力的Cep169消除了EB1相互作用和微管正端附着,表明Cep169是+TIPs的一个新成员。我们进一步表明,在U2OS细胞中异位表达Cep169或CDK5RAP2会诱导微管束集和乙酰化,而在HeLa细胞中敲低Cep169会诱导微管解聚,尽管CDK5RAP2将γ-微管蛋白组装到中心体上并不需要Cep169。这些结果表明,Cep169靶向微管末端并与CDK5RAP2一起调节微管的稳定性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/94e9/4613824/6ac4dd86b627/pone.0140968.g001.jpg

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