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A newly identified post-translational modification critical for learning

Synaptic plasticity is known to underlie learning and memory, but we’re still discovering the molecular mechanisms by which synaptic activity leads to changes in synapse morphology and function. A recent Nature Neuroscience paper reports a new post-translational modification that is required to coordinate



the changes involved in memory formation: after enhanced synaptic activity,DHHC5 palmitoylates catenin, increasing its binding to synaptic cadherin both in vitro and in the hippocampus of fear-conditioned rodents.


These researchers used a synthetic -catenin gene, in which the palmitoylated cysteine residues were mutated to serine, to demonstrate that -catenin palmitoylation is required for numerous facets of activity-induced synaptic plasticity, including N-cadherin stabilization at synapses, postsynaptic spine enlargement, insertion of GluA1 and GluA2 into the synaptic membrane, and increased mEPSC amplitude.


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