The microRNA miR-1 regulates a MEF-2-dependent retrograde signal at neuromuscular junctions

Cell. 2008 May 30;133(5):903-15. doi: 10.1016/j.cell.2008.04.035.

Abstract

We show that miR-1, a conserved muscle-specific microRNA, regulates aspects of both pre- and postsynaptic function at C. elegans neuromuscular junctions. miR-1 regulates the expression level of two nicotinic acetylcholine receptor (nAChR) subunits (UNC-29 and UNC-63), thereby altering muscle sensitivity to acetylcholine (ACh). miR-1 also regulates the muscle transcription factor MEF-2, which results in altered presynaptic ACh secretion, suggesting that MEF-2 activity in muscles controls a retrograde signal. The effect of the MEF-2-dependent retrograde signal on secretion is mediated by the synaptic vesicle protein RAB-3. Finally, acute activation of levamisole-sensitive nAChRs stimulates MEF-2-dependent transcriptional responses and induces the MEF-2-dependent retrograde signal. We propose that miR-1 refines synaptic function by coupling changes in muscle activity to changes in presynaptic function.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Caenorhabditis elegans / metabolism*
  • Caenorhabditis elegans Proteins / metabolism*
  • Levamisole / pharmacology
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Mutation
  • Neuromuscular Junction / metabolism*
  • Nicotinic Agonists / metabolism
  • Receptors, Nicotinic / metabolism
  • Signal Transduction*
  • Transcription Factors / metabolism*
  • Transcription, Genetic
  • rab3 GTP-Binding Proteins / metabolism

Substances

  • Caenorhabditis elegans Proteins
  • MicroRNAs
  • Nicotinic Agonists
  • Receptors, Nicotinic
  • Transcription Factors
  • UNC-29 protein, C elegans
  • Unc-63 protein, C elegans
  • mef-2 protein, C elegans
  • Levamisole
  • rab3 GTP-Binding Proteins