Cep44 functions in centrosome cohesion by stabilizing rootletin.

Delowar Hossain,Sunny Y.-P Shih,Julia White,William Y Tsang,Xintong Xiao

doi:10.1242/jcs.239616

Delowar Hossain, Sunny Y.-P Shih + Show 3 more

Open Access

https://doi.org/10.1242/jcs.239616

Copy DOI

Abstract

ABSTRACTThe centrosome linker serves to hold the duplicated centrosomes together until they separate in late G2/early mitosis. Precisely how the linker is assembled remains an open question. In this study, we identify Cep44 as a novel component of the linker in human cells. Cep44 localizes to the proximal end of centrioles, including mother and daughter centrioles, and its ablation leads to loss of centrosome cohesion. Cep44 does not impinge on the stability of C-Nap1 (also known as CEP250), LRRC45 or Cep215 (also known as CDK5RAP2), and vice versa, and these proteins are independently recruited to the centrosome. Rather, Cep44 associates with rootletin and regulates its stability and localization to the centrosome. Our findings reveal a role of the previously uncharacterized protein Cep44 for centrosome cohesion and linker assembly.

Highlights

The centrosome is the major microtubule-organizing center in higher eukaryotes (Bornens, 2012)
At late G2/early mitosis, the linker is dissolved through a process called centrosome disjunction, which allows the duplicated organelles to separate and migrate towards opposite poles for the establishment of the mitotic spindle
Cep44 is a novel protein localized to the proximal end of centrioles Recent proteomic analyses of human centrosomes have led to the identification of a large number of proteins, some of which remain uncharacterized (Andersen et al, 2003; Jakobsen et al, 2011)

Summary

Introduction

The centrosome is the major microtubule-organizing center in higher eukaryotes (Bornens, 2012). C-Nap1 localizes to the proximal end of mother and daughter centrioles, where it docks LRRC45 and rootletin. Nek2A phosphorylates several proteins including C-Nap1 (Fry et al, 1998a), rootletin (Bahe et al, 2005), LRRC45 (He et al, 2013), Cep68 (Fang et al, 2014), CCDC102B (Xia et al, 2018) and centlein (Fang et al, 2014), leading to their delocalization from the centrosome and subsequently linker dissolution.

Results

Conclusion