Researchers have discovered that a protein called ATSF-1, found deep within human cells, has an anti-aging function . This protein controls the delicate balance between the creation and repair of mitochondria, which are responsible for producing energy and maintaining cell youth.
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By boosting ATSF-1 function, cellular health was improved in a study using C. elegans. The discovery could have significant implications for healthy aging and the treatment of mitochondrial diseases.
At the University of Queensland, scientists have discovered that there is a protein inside human cells that has an anti-aging function. Associate Professor Steven Zuryn and Dr Michael Dai at the Queensland Brain Institute discovered that a protein called ATSF-1 controls a delicate balance between the creation of new mitochondria and the repair of damaged mitochondria.
Mitochondria, with their own DNA, produce energy within cells to power biological functions, but the toxic byproducts of this process contribute to the rate at which the cell ages.
"Under stress conditions, when mitochondrial DNA has been damaged, the ATSF-1 protein prioritizes repair that promotes cellular health and longevity," said Dr. Zuryn.
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“We studied ATFS-1 in C. elegans, or roundworms, and saw that enhancing its function promotes cellular health, which means the worms became more agile for a longer period.”
It is important to understand how cells promote repair, as this helps us identify potential interventions to prevent mitochondrial damage.
The ability to balance competing functional demands is crucial to ensure the survival of the organism. The transfer and repair of the mitochondrial genome (mtDNA) requires specific enzymatic activities. These processes may compete with each other, suggesting that this trade-off occurs continuously throughout our lives.
Through the study of Caenorhabditis elegans, it was discovered that the transcription factor bZIP ATFS-1/Atf5 regulates this balance in favor of mtDNA repair by locating in mitochondria and intervening in the assembly of the mitochondrial transcription complex before initiation between HMG-5/TFOM and RPOM-1/mtRNAP.
The use of ATFS-1 reduces age-dependent molecular damage to mtDNA via DNA glycosylase NTH-1/NTH1 and helicase TWNK-1/TWNK. This results in protecting cells from decreased activity and enhancing their functional lifespan.
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These findings showed that ATFS-1 acts as a molecular focal point for regulating the balance between genome expression and its maintenance in mitochondria.
