Biologists say the discovery of a new photoreceptor gene in fish, birds, and amphibians implies that mammals may have gone through a nocturnal phase in the course of evolution.

The recently discovered gene codes for melanopsin, a pigment that makes cells in the eye responsive to light and helps regulate circadian rhythms. The gene, found in non-mammalian vertebrates, matches the mammalian melanopsin gene. That match led researchers to conclude that a melanopsin gene previously found in frogs is missing from the mammalian genome. The paper, which suggests that mammals may have lost their second melanopsin gene over the course of evolution, was published in the August issue of the journal PLoS Biology.

Until now, researchers had considered the melanopsin genes in all vertebrates to be descended from a common ancestor, despite the wide dissimilarities they found between the mammalian and non-mammalian versions.

But the discovery of an entirely novel melanopsin gene in non-mammals presents a simple explanation for those dissimilarities: The two previously discovered melanopsin genes were not actually matches. It is the newly discovered gene that matches the mammalian one; the gene originally discovered in fish, birds, and amphibians has no corresponding sequence in the mammalian genome.

“Genes tend to be found in clusters,” said University of Virginia biologist Ignacio Provencio, whose team cloned the original melanopsin genes in 1998. “In mammals, this particular gene was missing from the corresponding cluster. That, to me, was really the most compelling part of the paper.”

Why humans and other mammals lost this gene along the evolutionary trek is still uncertain. Researchers believe it must have been very early on, perhaps when the first primitive dinosaurs walked the earth.

“The idea in the field is that because mammalian organisms went through a nocturnal phase, they lost some of these photoreceptors,” said Samer Hattar, a biologist and neuroscientist at Johns Hopkins University. “It may be…true, in the case of melanopsin, that we lost one form of the two that were available to us before the nocturnal bottleneck.”

This so-called mammalian bottleneck is controversial, but some scientists believe mammals underwent a selective process in which they lost many photoreceptive genes.

If so, it could explain why non-mammalian vertebrates have actually maintained two melanopsin genes while mammals have managed to lose one, dramatically reducing where and how much melanopsin is produced.

“Basically, the mammalian melanopsin is only expressed in a subset of retinal ganglion cells in the eye,” said biologist James Bellingham, who led the research team at the University of Manchester. “Whereas in non-mammalian vertebrates, it’s expressed in a wide variety of tissues in the brain and throughout the retina. It’s become a highly specialized gene in mammals.”
Studying the presence and activity of both melanopsin genes in species that have adapted to low-light conditions—such as snakes, geckos, and deep-sea fish—could provide answers as to why the two genes were maintained in vertebrates for hundreds of millions of years, but humans today make do with only one.

Simply finding out that two forms of melanopsin exist instead of just one is fascinating, Hattar said. “There is no doubt about it. It’s just very convincing data with a lot of potential.”

Originally published October 27, 2006


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