placed the batch of flies aside and began taking on a new group of test subjects.
But then something odd happened to that tainted sample of flies. “They wouldn’t die. A fruit fly usually lives for less than two months. And even then, within twenty-four hours or so, you begin seeing a handful of them drop. But none of the flies I injected with the vector dropped. Ever. They just kept flying around.”
Up until Otto’s serendipitous mistake, it was assumed that biological aging was controlled by hundreds, if not thousands, of separate genetic proteins found in the body—proteins that worked in concert to determine the rate of aging across various parts of an individual. “We always assumed that a thousand different internal mechanisms and external factors worked together to trigger the aging process,” says Dr. Phillip Frank, head of genetics at the National Institutes of Health. “When you think about it, you begin aging from the second you’re born. Our studies showed that specific proteins in your body activated all the different physiological processes and free radicals that go into both growing up and growing old. There was no master switch.”
Until Graham Otto came around.
The tainted fruit flies carried on living for weeks and weeks, with an apparently limitless supply of energy. The only dead fruit flies Otto found in the container were their offspring (the altered genes, Otto discovered, weren’t passed on), the offspring of their offspring, and the offspring of their offspring’s offspring. The original flies remained alive and fluttering about indefinitely. Otto acted quickly, retracing his footsteps from that late night in the lab, finding the supposedly unimportant protein he had mistakenly altered, and replicating the experiment again, without altering the original protein in the gene. Again, the flies had a seemingly indefinite lifespan.
The supposedly innocuous portion of the gene Otto had messed with turned out to be much more important than he had ever envisioned. He rushed to form his own independent biotech firm and called a lawyer to draft a patent for the protein. “Normally, this is something you do over the course of years,” he told Lack in an e-mail. “But we’re doing it in a week, because if we can replicate it across species, maybe there’s something there.” And replicate it he did, across mice, rats, guinea pigs, and others, including his own aging golden retriever, Buggle. In all instances, the altered animals appeared ageless when compared to their respective control groups, never growing old past the day the vector was introduced into their system. And all of them remain alive and well today, in tourist displays set up by the university—except for Buggle, who remains comfortably in the Otto household.
Despite his extroverted nature, Otto wasn’t known as a cocky, presumptuous man. The only careless thing he did in his life was to mistakenly alter the wrong gene in those fruit flies. So when he published his findings, he insisted only on reporting what he had found, and didn’t speculate on the potentially enormous worldwide impact of his research. Nevertheless, many in his field declared it junk science. “It just seemed like too easy of an answer,” says Dr. Frank. Still, while many questioned Otto’s findings, they didn’t hesitate to recreate his experiments. And they soon found that his discovery was everything he said it was. Far more than that, actually. “He understated the results because he didn’t want to sound like some kook. He refused to call it a cure for aging,” says Sarah Otto. “But that’s what it was, and the follow-up research proved it.”
To see if the same gene therapy worked in humans, Otto solicited an unlikely test group: patients with early-onset Alzheimer’s disease. “A disease like Alzheimer’s is triggered specifically by the advance of age,” Otto wrote in a subsequent e-mail to Lack. “So if we administer the cure to
But then something odd happened to that tainted sample of flies. “They wouldn’t die. A fruit fly usually lives for less than two months. And even then, within twenty-four hours or so, you begin seeing a handful of them drop. But none of the flies I injected with the vector dropped. Ever. They just kept flying around.”
Up until Otto’s serendipitous mistake, it was assumed that biological aging was controlled by hundreds, if not thousands, of separate genetic proteins found in the body—proteins that worked in concert to determine the rate of aging across various parts of an individual. “We always assumed that a thousand different internal mechanisms and external factors worked together to trigger the aging process,” says Dr. Phillip Frank, head of genetics at the National Institutes of Health. “When you think about it, you begin aging from the second you’re born. Our studies showed that specific proteins in your body activated all the different physiological processes and free radicals that go into both growing up and growing old. There was no master switch.”
Until Graham Otto came around.
The tainted fruit flies carried on living for weeks and weeks, with an apparently limitless supply of energy. The only dead fruit flies Otto found in the container were their offspring (the altered genes, Otto discovered, weren’t passed on), the offspring of their offspring, and the offspring of their offspring’s offspring. The original flies remained alive and fluttering about indefinitely. Otto acted quickly, retracing his footsteps from that late night in the lab, finding the supposedly unimportant protein he had mistakenly altered, and replicating the experiment again, without altering the original protein in the gene. Again, the flies had a seemingly indefinite lifespan.
The supposedly innocuous portion of the gene Otto had messed with turned out to be much more important than he had ever envisioned. He rushed to form his own independent biotech firm and called a lawyer to draft a patent for the protein. “Normally, this is something you do over the course of years,” he told Lack in an e-mail. “But we’re doing it in a week, because if we can replicate it across species, maybe there’s something there.” And replicate it he did, across mice, rats, guinea pigs, and others, including his own aging golden retriever, Buggle. In all instances, the altered animals appeared ageless when compared to their respective control groups, never growing old past the day the vector was introduced into their system. And all of them remain alive and well today, in tourist displays set up by the university—except for Buggle, who remains comfortably in the Otto household.
Despite his extroverted nature, Otto wasn’t known as a cocky, presumptuous man. The only careless thing he did in his life was to mistakenly alter the wrong gene in those fruit flies. So when he published his findings, he insisted only on reporting what he had found, and didn’t speculate on the potentially enormous worldwide impact of his research. Nevertheless, many in his field declared it junk science. “It just seemed like too easy of an answer,” says Dr. Frank. Still, while many questioned Otto’s findings, they didn’t hesitate to recreate his experiments. And they soon found that his discovery was everything he said it was. Far more than that, actually. “He understated the results because he didn’t want to sound like some kook. He refused to call it a cure for aging,” says Sarah Otto. “But that’s what it was, and the follow-up research proved it.”
To see if the same gene therapy worked in humans, Otto solicited an unlikely test group: patients with early-onset Alzheimer’s disease. “A disease like Alzheimer’s is triggered specifically by the advance of age,” Otto wrote in a subsequent e-mail to Lack. “So if we administer the cure to
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