Six predatory snake species on three continents, including three kinds of North American garter snakes, have independently developed a nearly identical molecular mechanism for resistance to a highly lethal defensive neurotoxin produced by the variety of amphibians they prey upon, according to researchers at the University of Virginia, University of Nevada, Utah State University and the University of Notre Dame.
A paper on the research is published this month in the journal Proceedings of the National Academy of Sciences.
The toxin – tetrodotoxin, or TTX – is more lethal than cyanide and can kill large mammals, including humans, even in small concentrations. But the snakes eat it up. This adaptation allows the snakes to regularly consume their favorite foods, species of newts and frogs that contain enough TTX to kill several people.
The snakes, which live in parts of North, Central and South America and Asia, have evolved a trait that allows them to resist the toxicity of their prey. 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,” said Edmund Brodie III, one of the study authors and a biology professor in U.Va.’s College of Arts & Sciences. “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 co-authors are Chris Feldman of the University of Nevada, Edmund Brodie Jr. of Utah State University and Michael Pfrender of the University of Notre Dame. The National Science Foundation funds the ongoing research.
