Science & Technology - Posted by Fariss Samarrai-Virginia on Monday, May 14, 2012 12:25 - 0 Comments    
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Trait lets snakes chow down on toxic newts

Frogs and newts, beware! Six snake species have independently developed a nearly identical molecular mechanism for resistance to a highly lethal defensive neurotoxin produced by their prey. Above, a North American garter snake eats a toxic newt. (Courtesy: University of Virginia)

U. VIRGINIA (US) — Six snake species on three continents have developed a similar trait to resist the poison of their highly toxic prey.


Several species of newts and frogs produce the toxin, known as tetrodotoxin, that is more lethal than cyanide.

The six snake species—including three kinds of North American garter snakes—have independently developed a nearly identical molecular mechanism for resisting the toxin, according to a study published in the Proceedings of the National Academy of Sciences.

Straight from the Source

Read the original study

DOI: 10.1073/pnas.1113468109

Tetrodotoxin, or TTX, attacks an organism by binding to sodium channels in the body’s cells, which interrupts electrical impulses in the muscles. Normally, this quickly results in paralysis and the death of any animal that ingests it.

The six snake species studied, however, have independently evolved an adaptation over millions of years that inhibits the toxin from binding to the sodium channels. What’s interesting to the researchers is that the mechanism for resistance is essentially the same in all six species, regardless of where they live or the kind of prey they eat.

“These results show us that evolution can be much more predictable than we previously thought,” says Edmund Brodie III, one of the study authors and a biology professor at the University of Virginia. “In evolving resistance to toxins, snakes still have to maintain basic nervous system function. Only a small number of mutations seem to prevent binding of the toxin but still allow nerves and muscles to carry out normal activities.”

Although other mutations are known to prevent the toxin from binding to sodium channels, those mutations must have had undesirable effects for the snakes. In other words, the single trait the snakes independently evolved—and passed on to each succeeding generation—is likely the best route to protecting them from the toxin without also harming them in some other way.

Brodie’s collaborators include researchers at the University of Nevada, Utah State University, and the University of Notre Dame. The National Science Foundation funds the ongoing research.

More news from the University of Virginia: www.virginia.edu/uvatoday

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