Electric organs help electric fish, like the electric eel, do all sorts of amazing things: they send and receive signals that sound like birdsong, helping them recognize other electric fish by species, sex and even individual. A new study in Science Advances explains how small genetic changes allowed electric fish to develop electric organs. This discovery could also help scientists identify the genetic mutations that cause certain human diseases.
Evolution took advantage of a quirk in fish genetics to develop electrical organs. All fish have duplicate versions of the same gene that produces tiny muscle motors called sodium channels. To evolve electric organs, electric fish turned off a duplicate of the sodium channel gene in muscles and turned it on in other cells. The tiny motors that typically cause muscles to contract have been repurposed to generate electrical signals, and voila! A new organ with astonishing capacities is born.
“It’s exciting because we can see how a small change in the gene can completely change where it’s expressed,” said Harold Zakon, professor of neuroscience and integrative biology at the University of Texas at Austin and corresponding author of the study.
In the new paper, researchers from UT Austin and Michigan State University describe the discovery of a short section of this sodium channel gene – about 20 letters long – that controls whether the gene is expressed in a given cell. . They confirmed that in electric fish, this control region is either impaired or completely absent. And that’s why one of the two sodium channel genes is turned off in the muscles of electric fish. But the implications go far beyond the evolution of electric fish.
“This control region is found in most vertebrates, including humans,” Zakon said. “So the next step in terms of human health would be to look at this region in human gene databases to see how much variation there is in normal people and if certain deletions or mutations in this region could lead to a reduced expression of sodium channels, which could lead to disease.
The study’s first author is Sarah LaPotin, a research technician in Zakon’s lab at the time of the research and currently a doctoral candidate at the University of Utah. In addition to Zakon, the study’s other lead authors are Johann Eberhart, professor of molecular biosciences at UT Austin, and Jason Gallant, associate professor of integrative biology at Michigan State University.
Zakon said the sodium channel gene had to be turned off in muscle before an electrical organ could evolve.
“If they turned on the gene in both the muscle and the electrical organ, then all the new things that happened to the sodium channels in the electrical organ would also happen in the muscle,” Zakon said. “So it was important to isolate gene expression in the electrical organ, where it could evolve without harming the muscle.”
There are two groups of electric fish in the world, one in Africa and the other in South America. The researchers found that electric fish from Africa had mutations in the control region, while electric fish from South America lost them entirely. Both groups arrived at the same solution to developing an electrical organ – losing expression of a sodium channel gene in muscle – albeit from two different routes.
“If you rewind the tape of life and play, would it play the same or find new ways to move forward? Would evolution work the same way over and over again? said Gallant, who breeds the South American electric fish that were used in part of the study. “Electric fish are trying to answer this question because they have repeatedly developed these incredible traits. We have swung for the fences in this article trying to figure out how these sodium channel genes have been repeatedly lost in electric fish. It was really a collaborative work.”
One of the next questions the researchers hope to answer is how the control region evolved to activate sodium channels in the electrical organ.
Funding for this research was provided by the National Science Foundation and the National Institutes of Health.
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