ZFIN ID: ZDB-PUB-130313-7
miR-153 Regulates SNAP-25, Synaptic Transmission, and Neuronal Development
Wei, C., Thatcher, E.J., Olena, A.F., Cha, D.J., Perdigoto, A.L., Marshall, A.F., Carter, B.D., Broadie, K., and Patton, J.G.
Date: 2013
Source: PLoS One   8(2): e57080 (Journal)
Registered Authors: Patton, James G., Thatcher, Elizabeth
Keywords: none
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
PubMed: 23451149 Full text @ PLoS One

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.