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Zebrafish do it. Why can’t we?

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Researchers briefly exposed zebrafish to intense light, which destroys the light receptors in their eyes, just as staring into the sun harms human eyes. But unlike humans, who remain blinded if the damage is severe enough, zebrafish repair the damage with new nerve cells.

U. MICHIGAN (US)—Biologists long have marveled at the ability of some animals to re-grow lost body parts—newts regrow legs and zebrafish re-grow fins—and even repair damaged heart and eye tissue. Now researchers have discovered that some of the same genes underlie the process in different types of tissues.

Using zebrafish as a model, researchers at the University of Michigan have found that genes involved in fin regeneration and heart repair are also required for rebuilding damaged light receptors in the eye, suggesting that a common molecular mechanism guides the process, no matter what body part is damaged. Findings were published in the Proceedings of the National Academy of Sciences.

The researchers briefly exposed zebrafish to intense light, which destroys the light receptors in their eyes, just as staring into the sun harms human eyes. But unlike humans, who remain blinded if the damage is severe enough, zebrafish repair the damage with new nerve cells (neurons).

Where do those new cells come from? The researchers suspected they develop from cells in the retina called Müller glia, known to have the ability to give rise to nerve cells.

Zhao Qin, a graduate student in the department of molecular, cellular, and developmental biology, wanted to find what prompts Müller glia to start the regeneration process. To get at the question, she looked at patterns of gene expression in Müller glia from damaged, regenerating zebrafish retinas and from undamaged zebrafish retinas to see which genes are expressed differently in damaged and undamaged retinas.

“Of course I found a lot of genes—a total of 953,” Qin says, “but two were of particular interest.” The two genes, hspd1 and mps1, had been found in other studies to be required for fin and heart regeneration in zebrafish, and Qin’s work showed that they also were switched on in Müller glia from damaged zebrafish retinas.

“This suggests,” says coauthor Pamela Raymond, “that, although we don’t fully understand it yet, there might be a bigger molecular program, involving not just these two genes but a number of cooperating genes that are required for injury-triggered regeneration.”

The researchers received funding from the National Institutes of Health.

University of Michigan news: www.umich.edu/news/

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