Mitochondrial peptide MOTS-c is a stress-induced signal that reprograms cell metabolism.
TOPICS DISCUSSED:
Mitochondrial Roles: Not just ATP production, but “speaker of the house” via communication molecules that “talk” to the rest of the cell.
Origin of Communication: Mitochondrial peptides were likely co-opted from ancient antimicrobial factors to synchronize nuclear and mitochondrial genomes.
MOTC Discovery: Identified in mitochondrial ribosomal RNA regions linked to interferon responses.
Stress Induction: MOTS-c is produced in response to exercise, immune activation, and nutrient withdrawal; circulates as a mitokine.
Nuclear Regulation: MOTS-c translocates to the nucleus under stress and acts as a nonspecific cofactor that shapes chromatin accessibility and gene expression.
Metabolic Effects: Prevents diet-induced obesity and fatty liver in mice without altering baseline weight; engages AMPK and suppresses anabolic pathways.
Immune Modulation: Shifts immune cell programs to reduce autoimmune attack in type 1 diabetes models.
Aging Phenotypes: Daily or intermittent dosing doubles running capacity and preserves walking ability in old mice.
ABOUT THE GUEST: Changhan David Lee, PhD is Associate Professor at the University of Southern California Leonard Davis School of Gerontology. His laboratory investigates mitochondrial communication and microproteins in the biology of aging.
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