Signals, synapses, and synthesis: how new proteins control plasticity.
Signals, synapses, and synthesis: how new proteins control plasticity.
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DOI：
10.3389/neuro.04.014.2009
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发表时间：
2009
影响因子：
3.5
通讯作者：
Bagni C
中科院分区：
文献类型：
--
作者：
Zukin RS;Richter JD;Bagni C
mRNA 的树突定位和局部蛋白质合成提供了基因表达的空间和时间调节，并赋予突触自主改变其结构和功能的能力。新的证据表明，RNA 结合蛋白、核糖体、翻译因子和编码对突触结构和功能至关重要的蛋白质的 mRNA 定位于神经元过程。 RNA 在翻译静止状态下被转运到树突中，并在树突中被突触刺激激活。调节树突状 RNA 传递和翻译抑制的两种 RNA 结合蛋白是细胞质多腺苷酸化元件结合蛋白和脆性 X 智力迟钝蛋白 (FMRP)。脆性 X 综合征 (FXS) 是自闭症最常见的已知遗传原因，其特征是 FMRP 缺失。 FXS 的标志性特征包括脊柱形态发生失调和代谢型谷氨酸受体依赖性长期抑郁（学习和记忆的细胞基质）。目前的研究重点是 mRNA 在翻译抑制状态下从体细胞转运到远端过程，并响应突触信号在突触位点被激活的机制。
Localization of mRNAs to dendrites and local protein synthesis afford spatial and temporal regulation of gene expression and endow synapses with the capacity to autonomously alter their structure and function. Emerging evidence indicates that RNA binding proteins, ribosomes, translation factors and mRNAs encoding proteins critical to synaptic structure and function localize to neuronal processes. RNAs are transported into dendrites in a translationally quiescent state where they are activated by synaptic stimuli. Two RNA binding proteins that regulate dendritic RNA delivery and translational repression are cytoplasmic polyadenylation element binding protein and fragile X mental retardation protein (FMRP). The fragile X syndrome (FXS) is the most common known genetic cause of autism and is characterized by the loss of FMRP. Hallmark features of the FXS include dysregulation of spine morphogenesis and exaggerated metabotropic glutamate receptor-dependent long term depression, a cellular substrate of learning and memory. Current research focuses on mechanisms whereby mRNAs are transported in a translationally repressed state from soma to distal process and are activated at synaptic sites in response to synaptic signals.
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