So, he said, "the marine fish actually carry the genes for this alternative state, but at such a low level it is never seen;" all the ocean fish remain well-armored. "But they do have this silent gene that allows this alternative form to emerge if the fish colonize a new freshwater location."
Also, comparing what happens to the ectodysplasin signaling molecule when its gene is mutated in humans, and in fish, shows a major difference. The human protein suffers "a huge amount of molecular lesions, including deletions, mutations, many types of lesions that would inactivate the protein," Kingsley said.
But in contrast, "in the fish we don't see any mutations that would clearly destroy the protein." There are some very minor changes in many populations, but these changes do not affect key parts of the molecule. In addition, one population in Japan used the same gene to evolve low armor, but has no changes at all in the protein coding region. Instead, Kingsley said, "the mutations that we have found are, we think, in the (gene's) control regions, which turns the gene on and off on cue." So it seems that evolution of the fish is based on how the Eda gene is used; how, when and where it is activated during embryonic growth.
Also, to be sure they're working with the correct gene, the research team used genetic engineering techniques to insert the armor-controlling gene into fish "that are normally missing their armor plates. And that puts the plates back on the sides of the fish," Kingsley said.
"So, this is one of the first cases in vertebrates where it's been possible to track down the genetic mechanism that controls a dramatic change in skeletal pattern, a change that occurs naturally in the wild," he noted.
"And it turns out that the mechanisms are surprisingly simple. Instead of killing the protein (with mutations), you merely adjust the way it is normally regulated. That allows you t
Source:Howard Hughes Medical Institute