There is a slender, striped snake found across North America that is exceedingly, if endemically, commonplace. It is the snake most likely to be seen near human habitation—two feet long, non-venomous, slithering among leaves in backyards or basking on sun-baked sidewalks in summer. Being an adaptable species, it dines eclectically and doesn’t mind sharing space with people (particularly if said people live near water), and these traits allow it to flourish wherever the climate suits. The reptile is so ubiquitous, its very name states as much: Common garter snake (Thamnophis sirtalis), the most pedestrian legless vertebrate on the continent. There is, however, one little detail that sets the garter snake apart, a dietary feat unmatched in all Animalia: It can eat rough-skinned newts whole, without dying. But this is jumping ahead a bit.
At first glance, the rough-skinned newt (Taricha granulosa) seems almost as workaday as the snake. One of the five most-common amphibians in Washington state—and probably the easiest to locate and identify—rough-skinned newts are found west of the Cascades from Alaska to Santa Cruz. They are diurnal, live on land, grow to eight inches in length, and amble about with almost laughable torpidity. Watching one prowl in slo-mo across the forest floor brings to mind a snub-nosed lizard, or possibly a pelycosaur. Brownish-black above and orange below, rough-skinned newts with their coppery eyes are not exactly awe-inspiring creatures to behold, but they command attention in a rather more serious way: their flesh is among the most noxious in the world. No North American animal crams as much toxicity into such an innocuous-looking package. Rattlesnakes, black widows, even the dreaded gila monster are bantamweights compared to the newt. The poison ingested from one adult male can kill at least seventeen humans—or roughly 25,000 laboratory mice—a potency 10,000 times greater than cyanide. Animals hapless enough to dine on newt often die on newt, sometimes so abruptly that the swallowed amphibian simply crawls back out of its assailant’s lifeless maw. Armed with such lethal defense, it’s no wonder that the rough-skinned newt can stumble around the forest in broad daylight, undaunted and impervious. Nothing in its right mind dares molest it—nothing, that is, except those common garter snakes. (Again, jumping ahead! Remember, patience is a virtue.)
Rough-skinned newts produce a chemical in their skin called tetrodotoxin, or TTX, a neurotoxin that blocks the brain’s nerve signals from reaching muscles. By glomming on to the sodium channels in nerve cells, TTX interferes with the flow of sodium ions into and out of each cell—an exchange necessary for normal muscle contraction—thereby paralyzing the tissue. If enough TTX is ingested, vessels dilate and blood pressure drops, leading swiftly to shock. The heart stops beating, the lungs cease to take air, and death is imminent, all as a result of this toxic signal-jamming.
TTX is produced by several other species of newt, as well as in pufferfishes and some kinds of poison-dart frog. In no other amphibian, though, is it found in such high concentrations as in the rough-skinned newt. In fact, some populations are so chock-full of the stuff that even the merest nibble by a typical newt-eating species—such as bullfrogs, raccoons, kingfishers, herons, domestic dogs and cats—would be fatal hundreds of times over. Why the overkill? Poison is costly to produce, after all, and it turns out that newts with especially high levels of TTX in their skin are actually more sluggish, perhaps as a result of residual toxicity. This overload would appear to work against the newts, but, like everything in nature, there are reasons for, well, everything.
If TTX seems the perfect foil to would-be predators, garter snakes have happened upon a perfect solution. In populations that prey regularly on rough-skinned newts, the snake’s neurons have evolved a shape of sodium channel incompatible with TTX molecules—that is, the toxin cannot readily attach itself to these malformed nerve cells, and thus cannot effect its paralysis on the snake’s muscles. Evolutionarily speaking, this is a show of one-upmanship between the two species, in which the mutations within the snake’s genes that conferred TTX-resistance—mutations that led to malformed sodium channels—place selective pressure on the newts to produce increasingly potent toxins. (Selective pressure can be described as any phenomena that alter the behavior or fitness of organisms in a given environment.) More toxins, in turn, trigger selective pressures that favor snakes with higher resistance, and so on through the generations.
Terms like “co-evolution” and “evolutionary arms race” seem at odds with one another—the former almost connotes a mutual dependence, while the latter suggests enmity and strife—but both are apt descriptors of this back-and-forth between the snake and the newt. They are inextricably bound, wherever their ranges overlap, and so must be viewed from a more holistic perspective: their shared struggle is greater than the mundanity of its parts. Both species are common, yes, but their intertwined lives offer a most uncommon glimpse into the intricacies of the natural world.