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YIF1A activates mTORC1 signaling to promote cellular senescence

Xiaogang Zhang1, Luying Liu2, Mengdi Shang3

  • 1School of Special Education and Rehabilitation, Shandong Medical and Pharmaceutical University, Yantai, China.

Cell Death & Disease
|June 23, 2026
PubMed

Insights

Researchers discovered YIF1A, a Golgi-localized protein, that regulates mTORC1 signaling by interacting with RNF126 to ubiquitinate G3BP1/2. This pathway impacts cellular senescence and aging.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • The mechanistic target of rapamycin complex 1 (mTORC1) is a key regulator of cellular metabolism and growth.
  • mTORC1 activation occurs at lysosomal and Golgi membranes, but Golgi-specific mechanisms are unclear.

Purpose of the Study:

  • To identify novel regulators of Golgi-associated mTORC1 signaling.
  • To elucidate the molecular mechanisms of YIF1A in mTORC1 activation.

Main Methods:

  • Yeast two-hybrid screening
  • Immunoprecipitation
  • Western blotting
  • siRNA knockdown
  • Cellular senescence assays
  • C. elegans lifespan assays

Main Results:

  • YIF1A was identified as a Golgi-localized protein that interacts with RNF126.
  • YIF1A and RNF126 promote K48-linked polyubiquitination of G3BP1/2, activating mTORC1.
  • Depletion of YIF1A or RNF126 stabilizes G3BP1/2 and inhibits mTORC1.
  • YIF1A knockdown confers resistance to etoposide/doxorubicin-induced senescence.
  • YIF-1 modulates lifespan in C. elegans.

Conclusions:

  • A novel Golgi-specific regulatory axis involving YIF1A, RNF126, and G3BP1/2 for mTORC1 activation was discovered.
  • YIF1A plays a role in cellular senescence and aging.
  • YIF1A is a potential therapeutic target for aging-related diseases.

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