Biomaterial Database

A new role of anterograde motor Kif5b in facilitating large clathrin-coated vesicle mediated endocytosis via regulating clathrin uncoating. 2018

Yan-Xiang Ni, and Nan Zhou, and Wen-Qian Xue, and Li Rong, and Wing-Ho Yung, and Rao-Zhou Lin, and Richard Yi-Tsun Kao, and Zhi-Gang Duan, and Hai-Tao Sun, and Hua-Rui Gong, and Xu-Ming Tang, and Meng-Fei Liu, and Wen Zhang, and Shuang Qi, and Sookja Chung, and You-Qiang Song, and Jian-Dong Huang

1School of Biomedical Sciences, The University of Hong Kong, Pokfulam, Hong Kong, SAR China.

Kif5b-driven anterograde transport and clathrin-mediated endocytosis (CME) are responsible for opposite intracellular trafficking, contributing to plasma membrane homeostasis. However, whether and how the two trafficking processes coordinate remain unclear. Here, we show that Kif5b directly interacts with clathrin heavy chain (CHC) at a region close to that for uncoating catalyst (Hsc70) and preferentially localizes on relatively large clathrin-coated vesicles (CCVs). Uncoating in vitro is decreased for CCVs from the cortex of kif5b conditional knockout (mutant) mouse and facilitated by adding Kif5b fragments containing CHC-binding site, while cell peripheral distribution of CHC or Hsc70 keeps unaffected by Kif5b depletion. Furthermore, cellular entry of vesicular stomatitis virus that internalizes into large CCV is inhibited by Kif5b depletion or introducing a dominant-negative Kif5b fragment. These findings showed a new role of Kif5b in regulating large CCV-mediated CME via affecting CCV uncoating, indicating Kif5b as a molecular knot connecting anterograde transport to CME.