a very unusual constellation of symptoms, and is passed as a unit through families."
Research had already shown that the Eda gene makes a protein, a signaling molecule called ectodermal dysplasin. This molecule is expressed in ectodermal tissue during development and instructs certain cells to form teeth, hair and sweat glands. It also seems to control the shape of - bones in the forehead and nose.
Now, Kingsley said, "it turns out that armor plate patterns in the fish are controlled by the same gene that creates this clinical disease in humans. And this finding is related to the old argument whether Nature can use the same genes and create other traits in other animals."
Ordinarily, "you wouldn't look at that gene and say it's an obvious candidate for dramatically changing skeletal structures in wild animals that end up completely viable and healthy,' he said. "Eda gene mutations cause a disease in humans, but not in the fish. So this is the first time mutations have been found in this gene that are not associated with a clinical syndrome. Instead, they cause evolution of a new phenotype in natural populations."
The research with the wild fish also shows that the same gene is used whenever the low armor trait evolves. "We used sequencing studies to compare the molecular basis of this trait across the northern hemisphere," said Kingsley. "It doesn't matter where we look, on the Pacific coast, the East coast, in Iceland, everywhere. When these fish evolve this low-armored state they are using the same genetic mechanism. It's happening over and over again. It makes them more fit in all these different locations."
Because this trait evolves so rapidly after ocean fish colonize new environments, he added, "we wondered whether the genetic variant (the mutant gene) that controls this trait might still exist in the ocean fish. So we collected large numbers of ocean fish with complete armor, and we found a very low level of this gene
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