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

PloS one | Mar 1, 2013

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.

Pubmed ID: 23451149 RIS Download

Mesh terms: 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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Associated grants

  • Agency: NICHD NIH HHS, Id: T32 HD007502
  • Agency: NIGMS NIH HHS, Id: GM 075790
  • Agency: NCRR NIH HHS, Id: RR12546
  • Agency: NIGMS NIH HHS, Id: T32 GM07347
  • Agency: NIGMS NIH HHS, Id: GM 54544
  • Agency: NINDS NIH HHS, Id: R01 NS038220
  • Agency: NEI NIH HHS, Id: EY019759
  • Agency: NINDS NIH HHS, Id: NS038220
  • Agency: NIGMS NIH HHS, Id: T32 GM08556
  • Agency: NIMH NIH HHS, Id: R01 MH096832
  • Agency: NIGMS NIH HHS, Id: T32 GM008554
  • Agency: NINDS NIH HHS, Id: F30 NS061403

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