Scientific Method / Science & Exploration

Placental mammals engaged in gene theft

Researchers find a part of a complex that lets charged atoms in and out of …

As any of you who remember back to when high-school biology covered osmosis, the balance of salts inside of cells can make the difference between life and death: too much, and the cell will explode; too little, and it will dry out and shrivel up. To keep everything under control, cells use what are called "ion channels" to regulate how the charged atoms of salts get into and out of cells. Ion channels can consist of one or more proteins that create a pore through the cell membrane, and their regulated activity is essential for not only cell health but for the control of the electrical charges that regulate muscle and nerve firing.

So, when researchers found a subunit of an ion channel (termed βm) that was expressed broadly in some animals, but only in the muscle cells of placental mammals, they probably thought they might be on to an interesting adaption, presumably involving the regulation of muscle activity. The were right that they were on to something interesting, but their recent publication suggests that any simple inference about how this protein regulates muscle activity is nowhere close to right.

One hint that something funny was going on came when the looked for where the protein is in the cell. Instead of being at the cell surface, βm appeared to never make it far from the area where it is first made, in the vicinity of the nucleus. Try as they might, the authors were also unable to detect the protein acting as part of a functional ion channel, either.

At a loss for what βm might be doing, they did a standard test to look for proteins that interacted with it. I can only imagine their surprise (and skepticism) when they pulled out SKIP, which is part of a complex of proteins that regulates gene expression in the nucleus. But, when tested with genes known to be regulated by SKIP, βm was found to be able to alter gene expression. So, its role in regulating muscle activity comes at the level of controlling which genes get expressed.

The authors suggest that somewhere along the lineage that lead to placental mammals, the βm gene stopped working as part of an ion channel, something made possible by the fact that there are four others like it in the genome to cover for it. Over time, it appears to have picked up additional mutations; the mammalian version has a string of charged amino acids at one end of the protein that may help it interact with other proteins and/or target it to the nucleus. It's not clear when this happened on the way to placental mammals. I took a quick look at a marsupial version of the gene, but it's only a partial sequence—there's no way to tell if the charged stretch is present.

The data are a great reminder that evolution really doesn't seem to involve much in the way of grand leaps or sudden changes. Rather, this sort of low-level genetic theft and tweaking seems to go on all the time; evolution appears to work more by tinkering with what exists than producing the entirely new.

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