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Naked mole-rats have special DNA protection. We could use AI to design something similar.
Four small differences in a single enzyme may help explain one of biology’s strangest outliers: the naked mole-rat’s ability to live for over thirty years without obvious signs of aging.
In a new Science paper, researchers in Shanghai, led by Zhiyong Mao, report that the naked mole-rat’s version of an enzyme called cGAS carries four amino-acid substitutions that appear to make its cells unusually good at repairing DNA damage, a primary hallmark of aging. When the team expressed the mole-rat version of cGAS in fruit flies, the flies lived about ten days longer - quite the extension for an animal that normally survives only two months.
It’s a modest evolutionary tweak with big consequences - one that might help explain why these rodents stay healthy long after other mammals their size are long gone.
“This is an excellent article,” Rochelle Buffenstein*, the biologist who first established naked mole-rats as models for studying aging, tells LEVITY.
“It makes sense - maintaining genomic integrity through efficient DNA repair will facilitate tissue homeostasis and good health.”
* If you want a crash course on naked mole-rat biology, don’t miss our LEVITY episode with Rochelle.
cGAS is best known as part of the immune system’s early-warning network. When it detects stray DNA, it sounds the alarm, calling in defenses against viruses or damaged cells. But in humans and mice, that vigilance comes at a price: inside the nucleus, cGAS interferes with the cell’s DNA-repair machinery, quietly accelerating the accumulation of genetic errors that drive aging.
“This is just one of many factors that add up”
The naked mole-rat’s version does the opposite. Those four amino-acid substitutions make the enzyme linger at the site of damage and cooperate with repair proteins instead of blocking them.
For Buffenstein, who has studied these animals for many decades, the discovery is exciting but not singular. “This is just one of many factors that add up,” she says. Other mutations known in the species - the loss of certain cell-death genes and a dampened inflammatory response - also seem to preserve the stability of its proteins and genome. “Many of these mutations seem to enhance proteostasis or genomic integrity and impact on promoting longevity and good health.”
Still, evolution rarely hands out free upgrades. Buffenstein notes that the same mutation helping cells repair themselves might also weaken immunity or raise cancer risk. “Naked mole-rats have no natural killer cells and are quite susceptible to viruses,” she says. “In the wild this may not be much of a problem, since they live in sealed burrows protected from pathogens.”
The cGAS change may also pose a different kind of risk in principle: steering cells toward repair rather than death can let damaged cells persist and divide. “Given that the mutation promotes DNA repair by homologous recombination rather than cell death,” Buffenstein says, “the sequence may lead to uncontrolled cell proliferation with a DNA mutation leading to cancer.” Naked mole-rats seem to buffer that risk with other safeguards; humans might not.
The real trick, then, isn’t simply repairing DNA better - it’s doing it without undermining apoptosis and immune surveillance. Could humans ever hope to reproduce that balance?
Perhaps. Mao’s team suggests that gene editing, mRNA delivery, or small-molecule drugs might someday nudge human cGAS to behave more like the mole-rat version. Buffenstein thinks AI-driven protein design could make that possible sooner than we expect. “With recent advances in protein design from generative AI,” she says, “it is possible that in the near future we may be able to design proteins to recapitulate the actions of naked mole-rat cGas”.
But as she also reminds us, cGAS is only one piece of a much larger puzzle. Most of the genes linked to the mole-rat’s resilience have clear counterparts in humans - the so-called orthologues - yet the newest, high-resolution “platinum” genomes reveal that others do not. These near-complete maps are uncovering sequences older methods missed: stretches of DNA with no known human equivalents. “The new platinum genomes recently published may lead to the identification of novel genes with no known orthologues that may play a bigger or key regulatory role,” she says.
In other words, some of the most important longevity levers might be unique to the mole-rat itself - a reminder that nature may have found solutions we don’t yet share, but that we might one day learn to imitate.
