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Regulation of cargo‐selective endocytosis by dynamin 2 GTP ase‐activating protein girdin
Author(s) -
Weng Liang,
Enomoto Atsushi,
Miyoshi Hiroshi,
Takahashi Kiyofumi,
Asai Naoya,
Morone Nobuhiro,
Jiang Ping,
An Jian,
Kato Takuya,
Kuroda Keisuke,
Watanabe Takashi,
Asai Masato,
IshidaTakagishi Maki,
Murakumo Yoshiki,
Nakashima Hideki,
Kaibuchi Kozo,
Takahashi Masahide
Publication year - 2014
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201488289
Subject(s) - dynamin , endocytosis , endocytic cycle , microbiology and biotechnology , clathrin , biology , signal transducing adaptor protein , gtp' , receptor mediated endocytosis , signal transduction , cell , biochemistry , enzyme
In clathrin‐mediated endocytosis ( CME ), specificity and selectivity for cargoes are thought to be tightly regulated by cargo‐specific adaptors for distinct cellular functions. Here, we show that the actin‐binding protein girdin is a regulator of cargo‐selective CME . Girdin interacts with dynamin 2, a GTP ase that excises endocytic vesicles from the plasma membrane, and functions as its GTP ase‐activating protein. Interestingly, girdin depletion leads to the defect in clathrin‐coated pit formation in the center of cells. Also, we find that girdin differentially interacts with some cargoes, which competitively prevents girdin from interacting with dynamin 2 and confers the cargo selectivity for CME . Therefore, girdin regulates transferrin and E‐cadherin endocytosis in the center of cells and their subsequent polarized intracellular localization, but has no effect on integrin and epidermal growth factor receptor endocytosis that occurs at the cell periphery. Our results reveal that girdin regulates selective CME via a mechanism involving dynamin 2, but not by operating as a cargo‐specific adaptor.