Jonathan, a giant tortoise thought to be 194 years old, has given scientists a first look at how a very old tortoise’s genes are switched on and off. Researchers in the US report that the genes his cells use to make energy carry fewer chemical signs of aging than other parts of his DNA1. The study was published in the journal Science Advances on October 72.
The finding comes from a single animal and a single cheek swab. It points to genes worth a closer look, not to a treatment for people.
What happened
Jonathan is an Aldabra giant tortoise who lives on St. Helena, a British island in the South Atlantic2. Scientists estimate he hatched around 1832, and he was brought to the island from the Seychelles in 1882 as a gift to Sir William Grey-Wilson, who later became its governor2. He was already fully grown when he arrived2. Guinness World Records lists him as the world’s oldest living land animal, and he is about 100 years older than other long-lived tortoises of his species2.
The team took a small tissue sample from the inside of his cheek and read his epigenome1. The epigenome is a layer of chemical on-off marks that sits on top of DNA. It controls which genes are active without changing the DNA itself1. One common mark is a small chemical tag called a methyl group: when it is attached, a gene tends to stay off, and when it falls off, the gene can turn on2. According to Chosun Biz, this is the first time a tortoise’s epigenome has been measured2.
The regions that had changed least with age were the “start switches” (promoters) of genes linked to mitochondria and to RNA handling1. Mitochondria are the small parts inside cells that produce energy. Their decline is considered one of the hallmarks of aging, and changes in the chemical signals that control them are thought to play a part1.
The evidence so far
To measure aging in the epigenome, the team used entropy, a measure of disorder borrowed from physics2. Young animals tend to have tidy, consistent switch patterns. Over time, marks fall off or attach in a messier way, and gene activity becomes less predictable2. Stephen Clark, who led the study, put it this way to Chosun Biz:
“If we have to define aging, it can be described as an increase in entropy.”2
As the researchers expected, Jonathan’s switch patterns overall were more disordered than those of 12- and 90-year-old tortoises2. But not everywhere. At 272 of 2,895 gene-control sites, his pattern looked like that of 5- and 12-year-old tortoises2. Those sites sit near genes that the team says play a key role in holding back aging2.
Justin Gerlach, a biologist at Peterhouse, University of Cambridge, and a co-author, said the gene regulators involved in energy production and DNA repair “have remained remarkably stable for nearly two centuries,” in Chosun Biz’s translation2. A-Z Animals quotes the same remark as “incredibly stable,” attributing it to a press release3.
The team also read Jonathan’s DNA sequence itself. They found 287 variants in aging-related genes that set him apart from other tortoises2. These are linked to repairing DNA damage, regulating metabolism and preventing cancer, and some involve protecting telomeres, the protective caps at the ends of chromosomes2.
How the sample was taken
The team first planned to draw blood, but the St. Helena government did not allow it because of infection concerns2. A-Z Animals reports that his caregivers feared a blood draw could harm him at his age3. Instead, researchers swabbed the inside of his mouth while feeding him, much like a COVID-19 test2. According to A-Z Animals, the first swab was contaminated with mouth bacteria, so a second one was taken3.
What it does not show yet
This is a study of one animal. It cannot tell whether the young-looking switches helped Jonathan live long, or whether they are simply something that happens to be true of him. Comparisons with a small number of younger tortoises cannot rule out chance.
Some coverage has gone further than the reported data. A-Z Animals headlined that Jonathan “has the cells of a 5-year-old” and wrote that his biological age is that of a five-year-old tortoise3. The figures reported by Chosun Biz paint a narrower picture: overall, his switch patterns were more disordered than in younger tortoises, and only a minority of sites (272 of 2,895) looked young2.
The sample type also limits the work. Cheek cells are only one tissue, and the researchers say blood samples are needed for more thorough sequencing1. An outside scientist, João Pedro de Magalhães of the University of Birmingham, said the team found new candidate genes linked to longevity, but that it first needs to be confirmed whether those genes really play the role suggested2.
Who is behind it
The study was led by Stephen Clark, president and chief scientist of the Kallel Foundation, a nonprofit in Tennessee focused on longevity research1. The European Animal Research Association names Vanderbilt Health as the other research partner1. Other coverage describes the team as coming from the University of Cambridge and the foundation3, and Gerlach is a fellow at Peterhouse, Cambridge2. The sources do not give details of how the work was funded.
The foundation has said it wants to run drug trials that companies avoid. The European Animal Research Association links the study to rapamycin, an existing drug that has been studied for possible anti-aging effects and that increases how efficiently mitochondria work1. Because it no longer has patent protection, there is little incentive for drug companies to test it in trials1. “As a nonprofit, we want to do clinical trials that no drug company wants to do,” Clark said1. The tortoise study itself did not test any drug.
Clark has also framed the work broadly. “Nature has already solved the riddle of aging in remarkable ways, and Jonathan’s genome provides a blueprint for cellular resilience,” he said, according to Chosun Biz2. That is the researchers’ interpretation, not something the data show directly.
How it fits the field
Giant tortoises have a slow metabolism, which researchers think may help explain why the species lives long in general3. Jonathan’s age suggests something more may be going on in his case3. Chosun Biz notes that other long-lived animals also carry DNA changes that help repair and prevent damage, and that what stood out here was how little some gene-control regions had aged2.
The link between mitochondria, gene switches and lifespan has been studied in other animals for years. In 2016, scientists at UC Berkeley and EPFL in Switzerland reported that mild stress on mitochondria early in life triggered lasting changes in gene switches in worms4. When they boosted the enzymes involved, the worms lived longer4. In mice, strains with the longest lifespans had much higher activity of these enzymes in the brain4. Those were worm and mouse studies and did not show the same in people.
A-Z Animals also points to a 2025 study of María Branyas Morera, a woman who lived to 117. Researchers did not find a single “longevity gene” but reported that she had healthier mitochondria in her immune cells than expected3. That was also a study of one person.
What to watch next
The researchers plan to study other long-lived species and to use blood samples, which would allow more thorough sequencing1. The main open question, as de Magalhães noted, is whether the candidate genes hold up when tested more directly2. Watch also for whether the Kallel Foundation moves ahead with the kind of drug trials Clark described, and whether other teams find similar young-looking gene switches in other very old animals.
