Tight Junction Component Occludin Binds to FIP5 to Regulate Endosome Trafficking and Mitotic Spindle Function

Author:

Zhang Zichao123,Chen Jing123,Ma Rongze123,Xu Chongshen123,Lu Yunzhe4,Zhou Jiecan5,Xia Kun12,Lu Pengfei123ORCID

Affiliation:

1. MOE Key Lab of Rare Pediatric Diseases Hengyang Medical School University of South China Hengyang China

2. Institute of Cytology and Genetics School of Basic Medical Sciences Hengyang Medical School University of South China Hengyang China

3. Institute for Future Sciences Hengyang Medical School University of South China Changsha China

4. School of Life Science and Technology ShanghaiTech University Shanghai China

5. The First Affiliated Hospital Hengyang Medical School University of South China Hengyang China

Abstract

AbstractThe genetic basis of vertebrate emergence during metazoan evolution has remained largely unknown. Understanding vertebrate‐specific genes, such as the tight junction protein Occludin (Ocln), may help answer this question. Here, it is shown that mammary glands lacking Ocln exhibit retarded epithelial branching, owing to reduced cell proliferation and surface expansion. Interestingly, Ocln regulates mitotic spindle orientation and function, and its loss leads to a range of defects, including prolonged prophase and failed nuclear and/or cytoplasmic division. Mechanistically, Ocln binds to the RabGTPase‐11 adaptor FIP5 and recruits recycling endosomes to the centrosome to participate in spindle assembly and function. FIP5 loss recapitulates Ocln null, leading to prolonged prophase, reduced cell proliferation, and retarded epithelial branching. These results identify a novel role in OCLN‐mediated endosomal trafficking and potentially highlight its involvement in mediating membranous vesicle trafficking and function, which is evolutionarily conserved and essential.

Funder

National Natural Science Foundation of China

Publisher

Wiley

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