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C. elegans S6K Mutants Require a Creatine-Kinase-like Effector for Lifespan Extension
Philip R McQuary1, Chen-Yu Liao2, Jessica T Chang3
1Development, Aging and Regeneration Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA; Graduate School of Biomedical Sciences, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Cell Reports
|March 1, 2016
Summary
Reduced S6 kinase (S6K) extends lifespan. This study identifies arginine kinase ARGK-1 as a key effector, potentially activating energy pathways and enhancing stress resistance in C. elegans.
Area of Science:
- Gerontology and Molecular Biology
- Biochemistry and Metabolism
Background:
- S6 kinase (S6K) deficiency is linked to extended lifespan across species.
- The precise molecular mechanisms driving S6K-mediated longevity remain largely unknown.
Purpose of the Study:
- To identify novel effectors of S6K-mediated longevity using a proteomics approach.
- To investigate the role of arginine kinase ARGK-1 in C. elegans aging and stress response.
Main Methods:
- Proteomics analysis of long-lived rsks-1/S6K mutant C. elegans.
- Gene expression and functional assays in C. elegans.
- Biochemical analysis of creatine kinase in mouse brain tissue.
Main Results:
- Arginine kinase ARGK-1 was identified as significantly enriched in rsks-1/S6K mutants.
- Overexpression of ARGK-1 extended C. elegans lifespan, partly via AAK-2/AMPK activation.
- ARGK-1 is essential for the reduced body size and enhanced stress resistance in rsks-1/S6K mutants.
- Increased creatine kinase levels were observed in S6K1 knockout mouse brains.
Conclusions:
- ARGK-1 acts as a specific effector of S6K-mediated longevity in C. elegans.
- ARGK-1 plays a role in regulating organismal size and stress resistance.
- Findings suggest a conserved role for creatine kinase pathway in aging and longevity.
