ATP availability influences lifespan in yeast cells
Mitochondria produce less energy as cells age. But is that energy loss a cause of aging, or merely a consequence? Scientists have now tested this directly in a living organism for the first time.
Researchers engineered a synthetic system in yeast cells (Saccharomyces cerevisiae). They used a transporter protein from a parasite to allow the cell to take up ATP from outside. ATP is the cell’s energy currency: the molecule produced during metabolism that powers virtually all cellular processes. The study was published in the journal eLife.
Less ATP shortened lifespan, more ATP extended it
When the researchers reduced ATP levels inside cells, yeast cells lived shorter lives. When they increased intracellular ATP by supplying it externally, cells expressing the transporter protein lived longer. The cells showed fewer features of a specific aging state linked to poorly functioning mitochondria, which the researchers call the mitochondrial dysfunction-associated aging state.
A second finding stood out: even yeast cells without the transporter protein lived longer when extra ATP was present in their environment. This points to an additional mechanism in which cells respond to ATP outside the cell. Transcriptomic analysis showed the two routes operated through distinct molecular processes.
Evidence, not a solution
This is a study in yeast cells. Yeast is a widely used model for basic processes in cellular aging, but findings do not automatically apply to human cells or organisms. The results do, however, provide the first direct evidence that cellular energy availability plays a causal role in determining how long a cell lives. Follow-up research is needed to determine whether similar mechanisms are active in animal or human cells.
Search terms to explore further: cellular energy homeostasis replicative lifespan, mitochondrial dysfunction yeast aging, ATP availability metabolic aging