A new role of anterograde motor Kif5b in facilitating large clathrin-coated vesicle mediated endocytosis via regulating clathrin uncoating
Autor: | Hai Tao Sun, Raozhou Lin, Meng Fei Liu, Wen Zhang, Xu Ming Tang, Wen Qian Xue, Yan Xiang Ni, Nan Zhou, Richard Y.T. Kao, You-Qiang Song, Wing-Ho Yung, Hua Rui Gong, Jian-Dong Huang, Li Rong, Shuang Qi, Sookja K. Chung, Zhi Gang Duan |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
biology Chemistry lcsh:Cytology Vesicle Mutant Cell Biology Endocytosis biology.organism_classification Biochemistry Clathrin Article Cell biology 03 medical and health sciences 030104 developmental biology Vesicular stomatitis virus Conditional gene knockout Genetics biology.protein Axoplasmic transport lcsh:QH573-671 Molecular Biology Intracellular |
Zdroj: | Cell Discovery Cell Discovery, Vol 4, Iss 1, Pp 1-13 (2018) |
ISSN: | 2056-5968 |
Popis: | 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. |
Databáze: | OpenAIRE |
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