ROBERT SIEGEL, Host:
From NPR News, this is ALL THINGS CONSIDERED. I'm Robert Siegel.
MELISSA BLOCK, Host:
NPR's Joe Palca explains.
JOE PALCA: David Kingsley studies how a small fish about three or four inches long, called the stickleback, adapted. Kingsley is a biologist at Stanford University.
DAVID KINGSLEY: We'd like to know what is it that's happened at the DNA level, the genetic level, in order to allow these organisms to colonize and then thrive in new environmental conditions.
PALCA: Turns out, the genetic changes aren't in genes that make things in the body. They're in bits of DNA that turn on and off the genes that makes things in the body. For example, consider how sticklebacks adapted to different predators. In a lake full of hungry trout, the successful stickleback will have lots of spines.
KINGSLEY: The sticklebacks would raise the spines. It's like trying to eat a pin cushion.
PALCA: But in other places, trout aren't the problem.
KINGSLEY: One of the other things that tries to eat sticklebacks are insects.
PALCA: Those must be big insects.
KINGSLEY: There's lots of insects in Canada that are bigger than sticklebacks.
KINGSLEY: Insects eat sticklebacks by grabbing onto the dorsal and the pelvic spines.
PALCA: And then burrowing in from the side. So the successful stickleback in an environment with lots of insects will have fewer spines for insects to grab on to. Kingsley looked at the fish with fewer spines and found something interesting: They still had the gene that makes the protein that makes the spines.
KINGSLEY: What's changed is not whether the gene exists, but where and when the gene is expressed.
PALCA: Geneticist Sean Carroll at the University of Wisconsin sees a similar phenomenon in fruit flies. In this week's print version of Science, he describes how one of these regulatory elements has caused fruit flies living at high altitudes to be darker than flies in the lowlands.
SEAN CARROLL: And that's occurred by a small number of mutations that have accumulated fairly recently in fruit flies living in East Africa.
PALCA: Once upon a time, the dogma was genes coded for proteins and proteins made the tissues, and enzymes and hormones that make us. But recently, Carroll says there's been increased interest in these regulatory elements; segments of DNA that don't actually code for proteins, but control the expression of the genes that do.
CARROLL: If we take a big picture of our genome, our DNA, only about one- and-a-half percent of the three billion letters in our DNA code for proteins. And we think that several more percent is involved in doing just this - of controlling how those genes that encode proteins are being used.
PALCA: In fact, those controlling bits of DNA have already helped explain some inherited conditions. Take lactose intolerance. People who can't digest milk as adults have the same protein coding gene as people who can. David Kingsley says what's changed is a regulatory element that decides when to switch off that gene.
KINGSLEY: You either only express that during the nursing period or you continue to express it into adulthood. And that simple change in how long is the milk digestion enzyme expressed is enough to make the difference between somebody who can enjoy ice cream or get sick when they try to eat it.
PALCA: Joe Palca, NPR News, Washington.
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