Research ArticleNeuroscience

The elongation factor eEF1A2 controls translation and actin dynamics in dendritic spines

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Science Signaling  13 Jul 2021:
Vol. 14, Issue 691, eabf5594
DOI: 10.1126/scisignal.abf5594

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Coordinated pause for plasticity

Protein synthesis and structural remodeling in dendritic spines mediate synaptic plasticity, the long-lasting changes in neuronal connectivity that underlie learning and memory. Protein synthesis appears to be initially suppressed in response to synaptic activity. Mendoza et al. found a common regulatory link that coordinates these processes. In mouse hippocampal neurons, glutamate-induced phosphorylation of the translation elongation factor eEF1A2 triggered its dissociation from its activator (the guanine exchange factor eEF1B), thereby transiently inhibiting protein synthesis. This phosphorylation event also triggered the dissociation of eEF1A2 from actin fibers, thereby facilitating actin motility and cytoskeletal remodeling. The findings provide mechanistic insight into how protein synthesis and structural remodeling are coordinated for synaptic plasticity.


Synaptic plasticity involves structural modifications in dendritic spines that are modulated by local protein synthesis and actin remodeling. Here, we investigated the molecular mechanisms that connect synaptic stimulation to these processes. We found that the phosphorylation of isoform-specific sites in eEF1A2—an essential translation elongation factor in neurons—is a key modulator of structural plasticity in dendritic spines. Expression of a nonphosphorylatable eEF1A2 mutant stimulated mRNA translation but reduced actin dynamics and spine density. By contrast, a phosphomimetic eEF1A2 mutant exhibited decreased association with F-actin and was inactive as a translation elongation factor. Activation of metabotropic glutamate receptor signaling triggered transient dissociation of eEF1A2 from its regulatory guanine exchange factor (GEF) protein in dendritic spines in a phosphorylation-dependent manner. We propose that eEF1A2 establishes a cross-talk mechanism that coordinates translation and actin dynamics during spine remodeling.

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