ARF6 and EFA6A regulate the development and maintenance of dendritic spines
ARF6 and EFA6A regulate the development and maintenance of dendritic spines
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DOI：
10.1523/jneurosci.4182-05.2006
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发表时间：
2006-05-03
影响因子：
5.3
通讯作者：
Kim, E
中科院分区：
文献类型：
--
作者：
Choi, S;Ko, J;Kim, E
树突棘发育和维持的细胞和分子机制尚未完全了解。ADP-核糖基化因子6（ARF 6）是一种小的GT3，已知调节肌动蛋白重塑和膜运输。在这里，我们报告参与ARF 6和交换因子ARF 6（EFA 6A）在脊柱发育和维护的调节。ARF 6的一种活性形式以破坏丝状伪足为代价促进树枝状棘的形成。EFA 6A以ARF 6激活依赖性方式促进棘形成。通过小干扰RNA敲低ARF 6和EFA 6A可减少棘形成。实时成像表明，ARF 6敲低降低了丝状伪足向棘的转化和早期棘的稳定性。ARF 6的促棘作用部分被Rac 1阻断。ARF 6和EFA 6A保护成熟的脊柱免受失活诱导的不稳定。这些结果表明，ARF 6和EFA 6A可能调节丝状伪足向棘的转化以及早期和成熟棘的稳定性。
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.