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mTOR Controls Mitochondrial Dynamics and Cell Survival via MTFP1
Masahiro Morita1, Julien Prudent2, Kaustuv Basu3
1Department of Biochemistry and Goodman Cancer Research Centre, McGill University, Montreal, QC H3A1A3, Canada; Department of Molecular Medicine and Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Molecular Cell
|September 19, 2017
Summary
The mechanistic target of rapamycin complex 1 (mTORC1) pathway controls mitochondrial fission via MTFP1. Inhibiting mTORC1 causes mitochondrial hyperfusion, impacting cell fate and apoptosis.
Area of Science:
- Cell Biology
- Molecular Biology
- Biochemistry
Background:
- Mitochondrial dynamics (fission/fusion), ATP production, and apoptosis are crucial cellular processes.
- The precise mechanisms linking environmental cues to mitochondrial functions remain unclear.
- The nutrient-sensing mTORC1 pathway plays a key role in cellular regulation.
Purpose of the Study:
- To elucidate the role of mTORC1 in regulating mitochondrial fission and apoptosis.
- To identify key mediators linking mTORC1 signaling to mitochondrial dynamics.
- To explore the therapeutic potential of modulating mTORC1 activity.
Main Methods:
- Investigated the effect of mTORC1 inhibition on mitochondrial morphology and apoptosis.
- Analyzed the translation and expression of mitochondrial fission process 1 (MTFP1).
- Utilized mTOR inhibitors and assessed the involvement of 4E-BPs and DRP1.
Main Results:
- mTORC1 stimulates MTFP1 translation, promoting mitochondrial fission and apoptosis.
- mTORC1 inhibition leads to MTFP1 downregulation and mitochondrial hyperfusion.
- MTFP1 acts as a critical effector of mTORC1, influencing cell fate decisions.
Conclusions:
- MTFP1 is a key effector linking mTORC1 signaling to mitochondrial fission and apoptosis.
- Modulating MTFP1 levels can switch mTOR inhibitor effects from cytostatic to cytotoxic.
- Targeting the mTORC1/MTFP1 axis offers potential therapeutic strategies for diseases involving apoptosis and mitochondrial dysfunction.
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