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REDD2-mediated inhibition of mTOR promotes dendrite retraction induced by axonal injury

B Morquette1, P Morquette2, J Agostinone1

  • 11] Department of Neuroscience, CHUM Research Center, University of Montreal, Montreal, QC, Canada [2] University of Montreal Hospital Research Center (CR-CHUM), Montreal, QC, Canada [3] Groupe de Recherche sur le Système Nerveux Central (GRSNC), University of Montreal, Montreal, QC, Canada.

Cell Death and Differentiation
|September 27, 2014
PubMed

Insights

Injury triggers REDD2 protein, inhibiting mTOR and causing dendritic defects in neurons. Restoring mTOR activity via REDD2 inhibition rescues dendrites and neuronal function, suggesting a therapeutic target for neurodegeneration.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Molecular Biology

Background:

  • Dendritic defects are hallmarks of neurodegenerative diseases with axonopathy.
  • Mechanisms underlying these dendritic changes after axonal injury remain poorly understood.

Purpose of the Study:

  • To investigate the molecular mechanisms regulating dendritic pathology following axonal injury.
  • To explore the role of the stress-induced protein REDD2 and mammalian target of rapamycin (mTOR) pathway in neuronal survival and function after injury.

Main Methods:

  • Utilized Thy1-YFPH mice subjected to optic nerve axotomy.
  • Employed short interfering RNA (siRNA) for REDD2 knockdown.
  • Performed whole-cell recordings to assess neuronal function.
  • Administered rapamycin to modulate mTOR activity.

Main Results:

  • Axonal injury induced REDD2 upregulation, inhibiting mTOR activity and causing RGC dendritic retraction.
  • REDD2 knockdown restored mTOR activity, rescuing dendritic morphology and complexity.
  • mTOR activation in RGCs via REDD2 depletion restored light response properties.
  • REDD2-dependent mTOR activity promoted RGC survival post-axonal damage.

Conclusions:

  • Injury-induced stress upregulates REDD2, leading to mTOR inhibition and subsequent dendrite pathology.
  • Targeting the REDD2-mTOR pathway offers a potential therapeutic strategy for neurodegenerative diseases involving axonopathy and dendritic defects.

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