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MTORC1 Regulates both General Autophagy and Mitophagy Induction after Oxidative Phosphorylation Uncoupling

Alberto Bartolomé1, Ana García-Aguilar2,3, Shun-Ichiro Asahara4

  • 1Naomi Berrie Diabetes Center and Department of Medicine, Columbia University, New York, New York, USA.

Molecular and Cellular Biology
|September 13, 2017
PubMed

Insights

Mechanistic target of rapamycin complex 1 (MTORC1) regulates mitochondrial health by controlling autophagy. Inhibiting MTORC1 restores the clearance of damaged mitochondria, crucial for cellular function.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Autophagy Research

Background:

  • Mechanistic target of rapamycin complex 1 (MTORC1) is a key negative regulator of autophagy.
  • The specific role of MTORC1 in clearing damaged mitochondria (mitophagy) is not fully understood.

Purpose of the Study:

  • To investigate whether MTORC1 regulates the autophagic clearance of damaged mitochondria.
  • To elucidate the mechanisms by which MTORC1 influences mitophagy.

Main Methods:

  • Utilized TSC2-deficient cells with constitutive MTORC1 activation.
  • Assessed autophagic flux, mitochondrial-protein aging, and p62/SQSTM1 accumulation.
  • Examined PINK1 and PARK2 translocation to damaged mitochondria.
  • Investigated the effects of MTORC1 inhibition and FoxO1 expression.

Main Results:

  • TSC2-/- cells exhibited impaired autophagic flux and increased mitochondrial-protein aging.
  • Accumulation of p62/SQSTM1-positive mitochondria and deficient mitophagy were observed.
  • MTORC1 inhibition or FoxO1 expression restored mitophagy and related molecular events.

Conclusions:

  • Intact MTORC1 signaling is essential for initiating general autophagy and PINK1/PARK2-mediated mitophagy.
  • MTORC1 regulates two synergistic processes vital for clearing damaged mitochondria.
Keywords:
MTORC1PINK1TSC2autophagymitophagyrapamycin

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