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Lynx Peptides

Animal & cell studies

MOTS-C

Metabolic and nuclear-stress experiments connect mitochondrial peptide origin with AMPK and transcriptional responses in cells and mice.

Research summary

MOTS-C is a 16-residue peptide encoded by a short open reading frame in the mitochondrial 12S ribosomal RNA region. “Mitochondrial-derived” describes its genetic origin. It does not mean that MOTS-C is a structural component of the respiratory chain. PMID 25738459

AMPK means AMP-activated protein kinase, an energy-sensing enzyme. The initial experiments connect MOTS-C with folate and purine metabolism and AMPK activation. Later cellular work examines stress-dependent movement into the nucleus and regulation of nuclear genes. Pathway activation, nuclear localisation and mouse metabolic outcomes are separate observations, not a demonstrated human outcome. PMID 25738459 · PMID 29983246

The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.

Cell metabolism 2015

Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P

Cell and mouse metabolic models

MOTS-C linked mitochondrial peptide signalling with folate and purine metabolism and AMPK activation in the initial cell experiments. Mouse work found prevention of age- and high-fat-diet-associated insulin resistance and diet-induced obesity. These results established a metabolic research direction, while the genetic origin and cellular mechanism remain distinct from the animal outcomes.

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The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress.

Cell metabolism 2018

Kim KH, Son JM, Benayoun BA, Lee C

Cellular stress and mouse models

MOTS-C moved into the nucleus during metabolic stress in cell experiments, with AMPK-dependent localisation and changes in stress-responsive gene expression. Under glucose restriction, the response involved antioxidant-response elements and interaction with NRF2-related transcriptional machinery. This gives a cellular explanation for mitochondrial–nuclear communication, rather than a measured clinical outcome.

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Models studied

  • Mitochondrial-derived peptide signalling
  • Cellular metabolic homeostasis
  • AMPK-linked stress responses
  • Mitonuclear communication

Key findings

  • Metabolism and AMPK

    Cellular folate–purine and AMPK observations underpin a distinct mitochondrial-peptide research programme with separate mouse metabolic findings.

  • Stress-responsive nuclear signalling

    Stress-dependent nuclear movement provides a cellular link between mitochondrial origin and transcriptional responses.

References

  1. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance.

    Cell metabolism 2015

    Lee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P

    PMID 25738459

    View on PubMed

  2. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress.

    Cell metabolism 2018

    Kim KH, Son JM, Benayoun BA, Lee C

    PMID 29983246

    View on PubMed

For laboratory research use only. Content is provided for research reference and is not intended as medical or veterinary guidance.