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Area of Science:

  • Cellular signaling
  • Metabolic homeostasis
  • Stress response

Background:

  • mTORC2 signaling regulates growth and survival but integrates stress signals poorly understood.
  • Mechanisms linking mTORC2, metabolism, and organismal survival under stress are unclear.

Purpose of the Study:

  • Investigate mTORC2's role in cold stress survival.
  • Elucidate the lipid-based signaling pathway downstream of mTORC2.

Main Methods:

  • Utilized genetic models to study mTORC2, SGK-1, S1P, PPARα/NHR-49, and ASM-3.
  • Analyzed lipid homeostasis, apoptosis, and neuronal damage under cold stress.

Main Results:

  • mTORC2 signaling reduces somatic lipid homeostasis, promoting apoptosis during cold stress via SGK-1.
  • Sphingosine-1-phosphate (S1P) acts as a cross-tissue survival signal.
  • S1P activates PPARα/NHR-49, repressing ASM-3 to prevent neuronal damage and promote survival.

Conclusions:

  • A novel lipid-based pathway downstream of mTORC2 couples stress and metabolic state to survival.
  • S1P mediates systemic survival decisions by signaling from lipid stores to neurons.