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MBC in Press, published online ahead of print March 7, 2007
Mol. Biol. Cell 10.1091/mbc.E06-08-0765

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Submitted on August 29, 2006
Revised on February 16, 2007
Accepted on February 28, 2007

R-Ras Regulates Exocytosis by Rgl2/Rlf-mediated Activation of RalA on Endosomes

Akiyuki Takaya,*{dagger} Takahiro Kamio,* Michitaka Masuda,{ddagger} Naoki Mochizuki,{ddagger} Hirofumi Sawa,{sect} Mami Sato,{sect} Kazuo Nagashima,{sect} Akiko Mizutani,|| Akira Matsuno,¶ Etsuko Kiyokawa,{dagger} and Michiyuki Matsuda*{dagger}

*Department of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Yamadaoka, Suita-shi, Osaka 565-0871, Japan; {dagger}Department of Pathology and Biology of Diseases, Graduate School of Medicine, Kyoto University, Kyoto 606-8501, Japan; {ddagger}Department of Structural Analysis, National Cardiovascular Center Research Institute, Suita-shi, Osaka 565-8565, Japan; {sect}Laboratory of Molecular and Cellular Pathology, Graduate School of Medicine, Hokkaido University, N15, W7, Kita-ku, Sapporo 060-8638, Japan; ||Basic Medical Science and Molecular Medicine, Tokai University School of Medicine, Isehara-shi, Kanagawa 259-1193, Japan; Department of Neurosurgery, Teikyo University Ichihara Hospital, Ichihara-shi, Chiba 299-0111, Japan

Monitoring Editor: Mark Ginsberg

R-Ras is a Ras-family small GTPase that regulates various cellular functions such as apoptosis and cell adhesion. Here we demonstrate a role of R-Ras in exocytosis. By the use of specific anti-R-Ras antibody, we found that R-Ras was enriched on both early and recycling endosomes in a wide range of cell lines. Using a fluorescence energy transfer (FRET)-based probe for R-Ras activity, R-Ras activity was found to be higher on endosomes than on the plasma membrane. This high R-Ras activity on the endosomes correlated with the accumulation of an R-Ras effector, the Rgl2/Rlf guanine nucleotide exchange factor for RalA, and also with high RalA activity. The essential role played by R-Ras in inducing high levels of RalA activity on the endosomes was evidenced by the shRNA-mediated suppression of R-Ras and by the expression of R-Ras GAP. In agreement with the reported role of RalA in exocytosis, the shRNA of either R-Ras or RalA was found to suppress calcium-triggered exocytosis in PC12 pheochromocytoma cells. These data revealed that R-Ras activates RalA on endosomes and that it thereby positively regulates exocytosis.

Address correspondence to: Michiyuki Matsuda (matsudam{at}path1.kyoto-u.ac.jp)




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