Neural plasticity depends on this long noncoding RNA's journ
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The brain constantly adapts to new information and stores memories by building connections among neurons, called synapses. How neurons do this reaching out arm-like dendrites to communicate with other neurons—requires a ballet of genes, signaling molecules, cellular scaffolding, and protein-building machinery. A new study finds a central role for one signaling molecule, a long, non-coding RNA that the scientists named ADEPTR.

Activity-dependent structural plasticity at the synapse requires specific changes in the neuronal transcriptome. While much is known about the role of coding elements in this process, the role of the long non-coding transcriptome remains elusive.

Here, researchers report the discovery of an intronic long noncoding RNA (lncRNA)—termed ADEPTR—that is up-regulated and synaptically transported in a cAMP/PKA-dependent manner in hippocampal neurons, independently of its protein-coding host gene. Loss of ADEPTR function suppresses activity-dependent changes in synaptic transmission and structural plasticity of dendritic spines.

Mechanistically, dendritic localization of ADEPTR is mediated by molecular motor protein Kif2A. ADEPTR physically binds to actin-scaffolding regulators ankyrin (AnkB) and spectrin (Sptn1) via a conserved sequence and is required for their dendritic localization.

Together, this study demonstrates how activity-dependent synaptic targeting of a lncRNA mediates structural plasticity at the synapse.

Science Advances
Source: https://advances.sciencemag.org/content/7/16/eabf0605
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