Engineering ATP import in yeast uncovers a synthetic route to extend cellular lifespan.

In engineered Saccharomyces cerevisiae expressing NTT1, intracellular ATP availability directly tunes replicative lifespan, with ATP depletion shortening and ATP supplementation restoring and extending it.

• Why it matters: Aging is linked to mitochondrial dysfunction and falling ATP, but whether ATP availability itself causally regulates lifespan has remained unresolved.
• What they did: The authors expressed a plasma membrane-targeted nucleotide transporter, NTT1, from Encephalitozoon cuniculi in yeast to deplete or import ATP independently of endogenous production, then measured replicative lifespan and performed transcriptomic and single-cell aging analyses.
• The result: NTT1-mediated ATP import suppresses glucose uptake, carbohydrate catabolism, mitochondrial respiration, and autophagy, while extracellular ATP triggers a distinct wild-type response; mitochondrial DNA–lacking cells show NTT1 effects require functional mitochondria, whereas extracellular ATP acts independently of mitochondrial respiration.

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