miR-153 Regulates SNAP-25, Synaptic Transmission, and Neuronal Development
- Authors
- 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.
- ID
- ZDB-PUB-130313-7
- 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.