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The Journal of Neuroscience, May 3, 2006, 26(18):4811-4819; doi:10.1523/JNEUROSCI.4182-05.2006

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Cellular/Molecular
ARF6 and EFA6A Regulate the Development and Maintenance of Dendritic Spines

Seungwon Choi,¹ Jaewon Ko,¹ Jae-Ran Lee,¹ Hyun Woo Lee,¹ Karam Kim,¹ Hye Sun Chung,² Hyun Kim,² and Eunjoon Kim¹

¹National Creative Research Initiative Center for Synaptogenesis and Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea, and ²Department of Anatomy and Division of Brain Korea 21 Biomedical Science, College of Medicine, Korea University, Seoul 136-705, Korea

Correspondence should be addressed to Eunjoon Kim, National Creative Research Initiative Center for Synaptogenesis and Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Kuseong-dong, Yuseong-ku, Daejeon 305-701, Korea. Email: kime{at}kaist.ac.kr

The cellular and molecular mechanisms underlying the development and maintenance of dendritic spines are not fully understood. ADP-ribosylation factor 6 (ARF6) is a small GTPase known to regulate actin remodeling and membrane traffic. Here, we report involvement of ARF6 and exchange factor for ARF6 (EFA6A) in the regulation of spine development and maintenance. An active form of ARF6 promotes the formation of dendritic spines at the expense of filopodia. EFA6A promotes spine formation in an ARF6 activation-dependent manner. Knockdown of ARF6 and EFA6A by small interfering RNA decreases spine formation. Live imaging indicates that ARF6 knockdown decreases the conversion of filopodia to spines and the stability of early spines. The spine-promoting effect of ARF6 is partially blocked by Rac1. ARF6 and EFA6A protect mature spines from inactivity-induced destabilization. These results suggest that ARF6 and EFA6A may regulate the conversion of filopodia to spines and the stability of both early and mature spines.

Key words: spine; filopodia; ARF6; EFA6A; Rac1; synapse

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Received Oct. 1, 2005; revised Feb. 28, 2006; accepted March 27, 2006.

Correspondence should be addressed to Eunjoon Kim, National Creative Research Initiative Center for Synaptogenesis and Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Kuseong-dong, Yuseong-ku, Daejeon 305-701, Korea. Email: kime{at}kaist.ac.kr

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