SMN regulates axonal local translation via miR-183/mTOR pathway

Hum Mol Genet. 2014 Dec 1;23(23):6318-31. doi: 10.1093/hmg/ddu350. Epub 2014 Jul 4.

Abstract

Reduced expression of SMN protein causes spinal muscular atrophy (SMA), a neurodegenerative disorder leading to motor neuron dysfunction and loss. However, the molecular mechanisms by which SMN regulates neuronal dysfunction are not fully understood. Here, we report that reduced SMN protein level alters miRNA expression and distribution in neurons. In particular, miR-183 levels are increased in neurites of SMN-deficient neurons. We demonstrate that miR-183 regulates translation of mTor via direct binding to its 3' UTR. Interestingly, local axonal translation of mTor is reduced in SMN-deficient neurons, and this can be recovered by miR-183 inhibition. Finally, inhibition of miR-183 expression in the spinal cord of an SMA mouse model prolongs survival and improves motor function of Smn-mutant mice. Together, these observations suggest that axonal miRNAs and the mTOR pathway are previously unidentified molecular mechanisms contributing to SMA pathology.

Publication types

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

MeSH terms

  • 3' Untranslated Regions
  • Animals
  • Axons / metabolism*
  • MicroRNAs / genetics
  • MicroRNAs / metabolism*
  • Muscular Atrophy, Spinal / metabolism
  • Muscular Atrophy, Spinal / pathology
  • Neurons / metabolism
  • Primary Cell Culture
  • Protein Biosynthesis*
  • RNA, Messenger / metabolism
  • Rats, Sprague-Dawley
  • Survival of Motor Neuron 1 Protein / genetics
  • Survival of Motor Neuron 1 Protein / metabolism*
  • TOR Serine-Threonine Kinases / biosynthesis*
  • TOR Serine-Threonine Kinases / genetics

Substances

  • 3' Untranslated Regions
  • MIRN183 microRNA, rat
  • MicroRNAs
  • RNA, Messenger
  • Smn1 protein, rat
  • Survival of Motor Neuron 1 Protein
  • mTOR protein, rat
  • TOR Serine-Threonine Kinases