Same Mutation Aided Evolution In Many Fish Species, Stanford Study Finds

In a diverse group of fish called the stickleback, nature took advantage of the same genetic trick time and again to allow freshwater species to shed their burdensome body armor and transform into a lighter, spryer fish. This is among the first times scientists have shown that the same genetic change is responsible for an evolutionary adaptation in disparate populations.

“Almost every time the stickleback evolves in fresh water it loses the armor,” said David Kingsley, PhD, professor of developmental biology and lead author of the study. “Although the trait evolved many times all over the world, nature uses the same gene each time.”

Sticklebacks evolved from a relatively uniform marine population into today’s broad spectrum of shapes and sizes when the last Ice Age ended roughly 10,000 years ago. Because ocean fish quickly evolved into such distinct populations when they colonized new freshwater lakes and streams, they are an ideal model for understanding how animals adapt to their unique environments.

The recent work carries a few surprises. Kingsley said that the gene in question, called Eda, is an old friend to laboratory researchers who have found that mutations in the same gene in mice cause altered hair patterns. However, in mice similar alterations can also be created by defects in any one of three different genes. “Based on the mouse work you’d predict we would find mutations in any of the three genes in sticklebacks,” said Kingsley, who is also a Howard Hughes Medical Institute investigator. “That’s not what we see.”

Instead, the group found the exact same genetic change in each of the 15 freshwater sticklebacks they studied, including one local species the group collected from a stream near Fresno. Perhaps mutations in the two other genes cause problems for the fish in addition to reducing the number of armor plates, Kingsley said.

Most of these fish evolved independently from marine ancestors that are covered head to hind fin in body armor. Although it’s not clear why losing the armor is a benefit to freshwater fish, Kingsley noted that the unarmored fish are lighter and faster than their more burdened marine cousins.

In an effort to learn more about how the armor trait evolves so quickly, Kingsley and his colleagues sequenced that genetic region in a large number of marine fish, all of which had a complete set of armor plates. A small number of these fish had one copy of the Eda gene that contained the mutation in question.

It’s likely that when a pocket of sticklebacks got isolated, at least a few of those fish already carried the mutated copy of the Eda gene. When those fish bred, some gave rise to offspring with two copies of the mutation and no (or reduced) body armor. In a freshwater habitat those fish prospered and populated the stream or lake with similarly armorless offspring.

Kingsley said this work is part of a larger study to understand how evolution generates major morphological and physiological changes. “We want to learn how evolution works on a large scale,” he said. In previous work, his group found that several species of stickleback lacking hind fins all shared an alteration in how a gene was turned on and off.

The striking similarity is that in both studies evolution turned to the same genetic switch to work a visible change in the fish. However, in the fin study the group wasn’t able to pinpoint the exact genetic alteration.

The group continues to wade out into nature, collecting additional stickleback species from around the world that can reveal whether particular genes are always reused when the animals adapt to new conditions, or if evolution has other tricks up its sleeve to push organisms towards an optimal form for their environment.

Other Stanford researchers who participated in the study include graduate students Pamela Colosimo, PhD, first author on the study, and Kim Hosemann; technician Sarita Balabhadra; undergraduate Guadalupe Villarreal Jr.; technical managers at the Stanford Human Genome Center Mark Dickson, Jane Grimwood and Jeremy Schmutz; and Richard Myers, PhD, professor of genetics.