If all you had to go on was our genomes, you’d surely conclude that humans and rodents were nearly the same animal, with roughly 92% overlap. And luckily for the species that does science, the other species is an excellent experimental tool, being small and cheap, with an easily replenishable stock. “How convenient for these large, hairless mammal-scientists,” you would think. Even cheaper are nematode worms and fruit flies (though only about 20% and 35% similar, respectively), and together with mice, these organisms have served as the substrate of thousands of biomedical discoveries in labs all over the world.
But although their short lives and high reproductive volume seem practically tailor-made for conducting longevity research, these animals are a particularly poor model of our own aging. This isn’t obvious from a purely genetic standpoint–most of the genes we’ve used to manipulate lifespan in the lab can be found in some form in humans. If nothing else, though, the magnitude of effect sizes alone–lifespan increases as large as 10x from a single mutation, in some cases–should stand out to us as almost unbelievable.
So should we
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