Arc mRNA Docks Precisely at the Base of Individual Dendritic Spines Indicating the Existence of a Specialized Microdomain for Synapse-Specific mRNA Translation
Arc mRNA Docks Precisely at the Base of Individual Dendritic Spines Indicating the Existence of a Specialized Microdomain for Synapse-Specific mRNA Translation
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DOI：
10.1002/cne.23073
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发表时间：
2012-10-01
影响因子：
2.5
通讯作者：
Steward, Oswald
中科院分区：
文献类型：
--
作者：
Dynes, Joseph L.;Steward, Oswald
Arc（又名 Arg 3.1）是由神经活动和学习经验引起的。 Arc mRNA 迅速输出到树突中，定位在激活的突触附近。通过对培养的活神经元中绿色荧光蛋白 (GFP) 标记的 mRNA 进行成像，我们发现包含 Arc 3'UTR（非翻译区）的融合转录本以极高的精度定位在树突棘底部的微域中。具有编码报告蛋白而不是 Arc 的 Arc 3'UTR 的转录本显示出精确的定位。在翻译抑制剂存在的情况下，本地化仍然存在，这表明本地化不需要持续翻译。同样，在用翻译抑制剂（嘌呤霉素）处理的脑组织中，多核糖体复合物仍稳定地定位在脊柱基部，该抑制剂可从 mRNA 中释放核糖体。单粒子追踪显示，位于脊柱基部的 Arc mRNA 粒子表现出高度受限的亚微米运动。这些观察结果表明，Arc mRNA 与以前未知的 mRNA 结合结构元件对接的脊柱基部存在微结构域。 J.Comp。内罗尔。 520:3105-3119, 2012。(C) 2012 Wiley 期刊公司。
Arc (aka Arg 3.1) is induced by neural activity and learning experience. Arc mRNA is rapidly exported into dendrites where it localizes near activated synapses. By imaging green fluorescent protein (GFP)-tagged mRNA in living neurons in culture, we show that fusion transcripts containing the Arc 3'UTR (untranslated region) localize with remarkable precision in a microdomain at the base of dendritic spines. Transcripts with the Arc 3'UTR that encode a reporter protein rather than Arc show precise localization. Localization persists in the presence of translation inhibitors, indicating that localization does not require ongoing translation. Similarly, polyribosome complexes remained stably positioned at spine bases in brain tissue treated with the translation inhibitor (puromycin) that releases ribosomes from mRNA. Single particle tracking revealed that Arc mRNA particles positioned at spine bases exhibited highly constrained submicron movements. These observations imply the existence of a microdomain at the spine base where Arc mRNA docks in association with a previously unknown mRNA-binding structural element. J. Comp. Neurol. 520:3105-3119, 2012. (C) 2012 Wiley Periodicals, Inc.