Dueling Endogenous Viral-Like Sequences Control Synaptic Plasticity

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The function of a large part of most genomes, generally called “junk DNA”, remains largely unknown. Much of this enigmatic DNA corresponds to transposons, which are considered genomic parasites. Here, we show the protein of the Ty1 retrotransposon Copia is enriched at the Drosophila neuromuscular junction and is transported across synapses. Unexpectedly, disrupting Copia expression results in increases in both synapse development and structural synaptic plasticity. Plasticity is kept in balance as Copia antagonizes the Drosophila Arc (activity-regulated cytoskeleton-associated protein) homolog, which is a transposon-derived gene. Our cryo-EM structure of the Copia capsid shows a shell with large cargo capacity and leads to a hypothesis for mutual antagonism of Arc and Copia capsid assembly. Our findings provide evidence that a fully functional transposon plays a role at synapses, suggesting that transposons and other types of ‘junk DNA’ are essential to developmental and cellular processes.

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  1. packages larger cargo

    Any idea whether it could be packaging anything else besides the mRNA and RTase or integrase that could be involved in synapse regulation?

  2. This suggests an exciting new example of TE domestication that relies on the “host’s” alternative splicing system

    This is fascinating. What do you know about the evolutionary history of Copia vs Arc? I was wondering this w the epistasis observation as well.