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Galectins Control mTOR in Response to Endomembrane Damage.

Jingyue Jia1, Yakubu Princely Abudu2, Aurore Claude-Taupin1

  • 1Autophagy Inflammation and Metabolism Center of Biomedical Research Excellence, University of New Mexico Health Sciences Center, 915 Camino de Salud, NE, Albuquerque, NM 87131, USA; Department of Molecular Genetics and Microbiology, University of New Mexico Health Sciences Center, 915 Camino de Salud, NE, Albuquerque, NM 87131, USA.

Molecular Cell
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PubMed
Summary

Lysosomal damage inhibits the mTOR pathway via galectin-8 (Gal8), activating autophagy and defense mechanisms. This discovery reveals a new galectin-based signaling system (GALTOR) that regulates mTOR in response to cellular injury.

Keywords:
AMPKAPEX2LC3TAK1TFEBautophagycatabolismgalectinslysosomemTOR

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Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Immunology

Background:

  • The mechanistic target of rapamycin (mTOR) kinase regulates metabolic pathways, including autophagy.
  • Autophagy is crucial for maintaining cellular and organelle homeostasis, beyond its catabolic roles.
  • The signaling mechanisms linking endomembrane damage to mTOR-mediated autophagic responses remain unclear.

Purpose of the Study:

  • To investigate how lysosomal damage signals are transmitted to mTOR to regulate autophagy.
  • To identify the molecular players involved in sensing lysosomal damage and initiating cellular responses.

Main Methods:

  • Investigated the role of galectins in sensing lysosomal damage.
  • Examined the association of galectins with the mTOR signaling complex on lysosomes.
  • Analyzed the impact of lysosomal damage on mTOR activity, AMPK activation, and downstream effectors like autophagy.

Main Results:

  • Lysosomal damage inhibits mTOR activity, mediated by the association of galectin-8 (Gal8) with the lysosomal mTOR apparatus.
  • Galectin-8 inhibits mTOR via the Ragulator-Rag signaling pathway.
  • Galectin-9 activates AMP-activated protein kinase (AMPK) in response to lysosomal injury, converging with mTOR pathways on autophagy and defense against Mycobacterium tuberculosis.

Conclusions:

  • A novel galectin-based signal-transduction system, termed GALTOR, has been identified.
  • GALTOR intersects with known mTOR regulators at the lysosome, controlling cellular responses to damage.
  • This pathway is critical for orchestrating autophagy and immune defense following lysosomal injury.