miR-153 Regulates SNAP-25, Synaptic Transmission,and Neuronal Development |
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| Authors: | Chunyao Wei Elizabeth J Thatcher Abigail F Olena Diana J Cha Ana L Perdigoto Andrew F Marshall Bruce D Carter Kendal Broadie James G Patton |
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| Institution: | 1. Department of Biological Sciences, Vanderbilt University and Medical School, Nashville, Tennessee, United States of America.; 2. Department of Biochemistry, Vanderbilt University and Medical School, Nashville, Tennessee, United States of America.; Wake Forest University, United States of America, |
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| 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. |
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