miR-153 regulates SNAP-25, synaptic transmission, and neuronal development.

Wei C, Thatcher EJ, Olena AF, Cha DJ, Perdigoto AL, Marshall AF, Carter BD, Broadie K, Patton JG
PLoS One. 2013 8 (2): e57080

PMID: 23451149 · PMCID: PMC3581580 · DOI:10.1371/journal.pone.0057080

SNAP-25 is a core component of the trimeric SNARE complex mediating vesicle exocytosis during membrane addition for neuronal growth, neuropeptide/growth factor secretion, and neurotransmitter release during synaptic transmission. Here, we report a novel microRNA mechanism of SNAP-25 regulation controlling motor neuron development, neurosecretion, synaptic activity, and movement in zebrafish. Loss of miR-153 causes overexpression of SNAP-25 and consequent hyperactive movement in early zebrafish embryos. Conversely, overexpression of miR-153 causes SNAP-25 down regulation resulting in near complete paralysis, mimicking the effects of treatment with Botulinum neurotoxin. miR-153-dependent changes in synaptic activity at the neuromuscular junction are consistent with the observed movement defects. Underlying the movement defects, perturbation of miR-153 function causes dramatic developmental changes in motor neuron patterning and branching. Together, our results indicate that precise control of SNAP-25 expression by miR-153 is critically important for proper neuronal patterning as well as neurotransmission.

MeSH Terms (11)

Animals Base Sequence Exocytosis Green Fluorescent Proteins MicroRNAs Motor Neurons Sequence Homology, Amino Acid Signal Transduction Synaptic Transmission Synaptosomal-Associated Protein 25 Zebrafish

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