Reciprocal interaction with G-actin and tropomyosin is essential for aquaporin-2 trafficking

Journal of Cell Biology - Tập 182 Số 3 - Trang 587-601 - 2008
Yumi Noda1,2, Saburo Horikawa3, Eiichiro Kanda1, M. Yamashita1, Hu Meng1, Kayoko Eto1, Yuhua Li1, Michio Kuwahara1, Keiji Hirai4, Chan‐Gi Pack5, Masataka Kinjo5, Shigeo Okabe6, Sei Sasaki1
11Department of Nephrology and
22COE Program for Brain Integration and its Disorders, Graduate School of Medicine, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo 113-8519, Japan
33Division of Pathophysiology and
44Department of Autonomic Physiology, Medical Research Institute, Tokyo Medical and Dental University, Bunkyo-ku, Tokyo, 113-8510 Japan
55Laboratory of Supramolecular Biophysics, Research Institute for Electronic Science, Hokkaido University, N12W6, Kita-Ku, Sapporo 060-0812, Japan
66Department of Cellular Neurobiology, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo 113-0033, Japan

Tóm tắt

Trafficking of water channel aquaporin-2 (AQP2) to the apical membrane and its vasopressin and protein kinase A (PKA)–dependent regulation in renal collecting ducts is critical for body water homeostasis. We previously identified an AQP2 binding protein complex including actin and tropomyosin-5b (TM5b). We show that dynamic interactions between AQP2 and the actin cytoskeleton are critical for initiating AQP2 apical targeting. Specific binding of AQP2 to G-actin in reconstituted liposomes is negatively regulated by PKA phosphorylation. Dual color fluorescence cross-correlation spectroscopy reveals local AQP2 interaction with G-actin in live epithelial cells at single-molecule resolution. Cyclic adenosine monophosphate signaling and AQP2 phosphorylation release AQP2 from G-actin. In turn, AQP2 phosphorylation increases its affinity to TM5b, resulting in reduction of TM5b bound to F-actin, subsequently inducing F-actin destabilization. RNA interference–mediated knockdown and overexpression of TM5b confirm its inhibitory role in apical trafficking of AQP2. These findings indicate a novel mechanism of channel protein trafficking, in which the channel protein itself critically regulates local actin reorganization to initiate its movement.

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Thông tin xuất bản

Journal of Cell Biology

Tập 182 Số 3

587-601

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