Synaptic plasticity involves structural modifications in dendritic spines. Increasing evidence suggests that structural plasticity is modulated by local protein synthesis and actin remodeling in a synapsis-specific manner. However, the precise molecular mechanisms connecting synaptic stimulation to these processes in dendritic spines are still unclear. In the present study, we demonstrate that the configuration of phosphorylation sites in eEF1A2, an essential translation elongation factor in neurons, is a key modulator of structural plasticity in dendritic spines. A mutant that cannot be phosphorylated stimulates translation but reduces actin dynamics and spine density. By contrast, the phosphomimetic variant loosens its association with F-actin and becomes inactive as a translation elongation factor. Metabotropic glutamate receptor signaling triggers a transient dissociation of eEF1A2 from its GEF protein in dendritic spines, in a phospho-dependent manner. We propose that eEF1A2 establishes a crosstalk mechanism that coordinates local translation and actin dynamics during spine remodeling

中文翻译：

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eEF1A2控制结构突触可塑性中的局部翻译和肌动蛋白动力学

突触可塑性涉及树突棘的结构修饰。越来越多的证据表明，结构可塑性受突触特异方式的局部蛋白质合成和肌动蛋白重塑的调节。然而，将突触刺激与树突棘的这些过程联系起来的精确分子机制仍不清楚。在本研究中，我们证明了eEF1A2中的磷酸化位点的配置是神经元中必不可少的翻译延伸因子，是树突棘结构可塑性的关键调节剂。不能被磷酸化的突变体刺激翻译，但是降低了肌动蛋白的动力学和脊柱密度。相比之下，拟磷酸酶变体失去了其与F-肌动蛋白的结合，并失去了翻译延伸因子的活性。促代谢型谷氨酸受体信号以磷酸依赖性方式触发树突棘中eEF1A2从其GEF蛋白的瞬时解离。我们建议eEF1A2建立一个串扰机制，以协调脊柱重塑过程中的局部翻译和肌动蛋白动力学