A new study in Nature Aging led by Prof. Chonglin Yang and colleagues has revealed a previously unknown mechanism that helps cells protect their powerhouses—mitochondria—during stress and aging.
The team discovered Mitochondria-Associated Translation Organelles (MATOs), a novel class of membraneless condensates formed by liquid–liquid phase separation (LLPS). These structures assemble directly on the mitochondrial surface, where they act as local protein factories.
At the center of this process is the RNA-binding protein LARP-1, which brings together ribosomes, mRNAs, and other RNA-binding proteins to produce crucial components for mitochondrial energy production and structure, such as IMMT-1 (a MICOS complex subunit for cristae organization) and ATP-2 (a key subunit of ATP synthase).
Using C. elegans as a model, the researchers showed that:
- Loss of LARP-1 or MATOs disrupts cristae organization, reduces ATP output, and shortens lifespan.
- By contrast, keeping MATOs anchored to mitochondria during stress or aging preserves mitochondrial function and significantly extends lifespan.
Mitochondrial decline is a hallmark of aging and contributes to neurodegeneration and metabolic disease. This discovery shows that biomolecular condensates directly regulate mitochondrial health, suggesting that stabilizing MATOs could become a new therapeutic strategy to combat age-related dysfunction.