 As you've probably noticed, some people develop gray hairs earlier than others, and centenarians tend to run in families. In other words, we don't all age at the same rate. Some of us will grow up to be active 90-year-olds running marathons, and others will have degenerative diseases in our 50s. Some of these genetic features are due to environmental influences, such as diet, stress, and exercise. But can the environment alone explain all of these differences in how quickly we age? The short answer is no. The environment alone cannot explain everything when it comes to aging. Then what else could be contributing? In the early 1990s, the idea that aging could be in our genes was hard to imagine, but Cynthia Kenyon from the University of California in San Francisco thought it may be possible. During a geneticist, she knew that most processes were controlled by genes. So she thought these differences in the rate at which we age might also be genetically controlled. Dr. Kenyon attempted to find the genes responsible for aging in humans. Aging in this case was defined as the organism's lifespan, as well as the rate at which it experienced physical decline. Perhaps there is one or a set of genes whose activity controls the rate of aging. Maybe these genes are activators of aging. When they are highly active, for example, aging may take place more quickly. Or perhaps it's the other way around. Maybe these genes negatively regulate aging. When they are active, aging may take place more slowly. Dr. Kenyon's laboratory used a model organism to find the genes responsible for aging, the worm C. elegans. C. elegans are small, simple organisms with a lifespan of 2-3 weeks. This rapid life cycle makes the study of aging much more feasible. In order to determine if something is controlled by genes, scientists introduce mutations or modifications to genes and examine the response. In this case, scientists randomly made mutations to genes in the C. elegan worm. Specifically, they used a clever technique called temperature-sensitive mutations. While the worm's DNA always contains the mutation, the protein produced from that DNA behaves normally at lower temperatures, but it does not function correctly when the worms are at higher temperatures. So what the scientists did was grow their worms at a normal temperature of 15 degrees Celsius so the mutations would not take effect. And then, after the worms progressed through their development, the scientists shifted the worms to a higher temperature of 20 degrees Celsius. At this higher temperature, the mutations took effect. They then tracked the lifespan of these worms and found that at the higher temperature, some worms lived twice as long as others. These long-lived worms had mutations in the DAF2 gene that caused the DAF2 protein to be non-functional. These mutations doubled their lifespan. The long-lived worms weren't just going in the nursing home and hanging on. They were living longer and healthier. They were still fertile, able to feed properly and very active. They simply seemed to age more slowly. This was incredible, nothing like it had ever been seen before, and no one thought this would be possible. The scientists had found a gene, one single gene, that when modified, delayed aging. But what is DAF2? And does DAF2 control aging in humans like it does in worms? The DAF2 protein is a receptor that responds to insulin-like signals. When conditions are favorable for the C. elegans worm, like when there's a lot of food around, signals through DAF2 regulate growth metabolism and energy storage. When DAF2 is non-functional, the worm doesn't get growth signals and sees the environment as dangerous. In response to these perceived dangerous signals, the C. elegans turn on protective pathways to ensure their cells and DNA remain healthy, thereby delaying aging. DAF2 is a conserved gene that is also found in many other species, including mice, flies and humans. When DAF2 is non-functional, mice and flies live longer as well. In humans, certain populations of Ashkenazi Jews that have many centenarians also have less functional DAF2. This would suggest that DAF2 can also control rates of aging in our species as well. These findings were published in 1993 in Nature in an article titled A C. elegans mutant that lives twice as long as wild type. Thanks to these genetic experiments, scientists could begin studying the molecular mechanism of aging. Since this research, we have gained insight into the genetics of aging. Why do some of us age more quickly than others? Can we intervene with these pathways to delay or even prevent the effects of aging? These questions and the answers they will continue to generate may be used to identify certain interventions that may delay or slow aging and increase our health span, our ability to live healthy and active lives for longer. This video has been provided to you by Eureka Science and iBiology, bringing the world's best biology to you.