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

PLoS One. 2013;8(2):e57080. doi: 10.1371/journal.pone.0057080. Epub 2013 Feb 25.

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Base Sequence
  • Exocytosis / physiology
  • Green Fluorescent Proteins / genetics
  • MicroRNAs / genetics
  • MicroRNAs / physiology*
  • Motor Neurons / cytology*
  • Sequence Homology, Amino Acid
  • Signal Transduction / physiology
  • Synaptic Transmission / physiology*
  • Synaptosomal-Associated Protein 25 / physiology*
  • Zebrafish / embryology

Substances

  • MicroRNAs
  • Synaptosomal-Associated Protein 25
  • Green Fluorescent Proteins