ARF6和EFA6A调节树突棘的发育和维持。
ARF6 and EFA6A regulate the development and maintenance of dendritic spines.
作者信息
Choi Seungwon, Ko Jaewon, Lee Jae-Ran, Lee Hyun Woo, Kim Karam, Chung Hye Sun, Kim Hyun, Kim Eunjoon
机构信息
National Creative Research Initiative Center for Synaptogenesis, Department of Biological Sciences, Korea Advanced Institute of Science and Technology, Daejeon 305-701, Korea.
出版信息
J Neurosci. 2006 May 3;26(18):4811-9. doi: 10.1523/JNEUROSCI.4182-05.2006.
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.
树突棘发育和维持背后的细胞及分子机制尚未完全明确。ADP核糖基化因子6（ARF6）是一种已知可调节肌动蛋白重塑和膜运输的小GTP酶。在此，我们报告ARF6及其交换因子EFA6A参与树突棘发育和维持的调控。ARF6的活性形式以丝状伪足为代价促进树突棘的形成。EFA6A以ARF6激活依赖的方式促进树突棘形成。通过小干扰RNA敲低ARF6和EFA6A会减少树突棘形成。实时成像表明，敲低ARF6会减少丝状伪足向树突棘的转变以及早期树突棘的稳定性。ARF6促进树突棘的作用部分被Rac1阻断。ARF6和EFA6A可保护成熟树突棘免受失活诱导的不稳定影响。这些结果表明，ARF6和EFA6A可能调节丝状伪足向树突棘的转变以及早期和成熟树突棘的稳定性。
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