Rough-skinned newt

The rough-skinned newt (Taricha granulosa) lives along North America’s Pacific coast, from Alaska down to Santa Cruz, California. It’s stocky, with a rounded snout, and its back ranges from light brown to olive or brownish-black, while its underside—including head, legs, and tail—is a bright orange to yellow. The skin is usually bumpy, but males become smooth-skinned during breeding season. Adults measure 6 to 9 cm from snout to vent, and 11 to 18 cm overall. They resemble California newts but have smaller eyes, yellow irises, V-shaped tooth patterns, and uniformly dark eyelids. During breeding, males can be told apart by their swollen vent lobes and rough toe pads. The species is rare east of the Cascade Mountains, though some populations—such as one near Moscow, Idaho—are thought to be introduced. Two subspecies were once widely recognized: *Taricha granulosa* and *Taricha granulosa mazamae* (the Crater Lake newt), but the latter is now considered invalid because similar-looking newts have been found in Alaska.

The newt’s skin glands produce a potent toxin, tetrodotoxin (formerly called tarichatoxin), which is the same poison found in pufferfish and other marine animals. The toxin is made by the newt’s skin microbiome and gives off a sharp, acrid smell that warns predators away. Poisoning usually only happens if the newt is eaten, though skin irritation—especially if eyes are touched after handling—has been reported. In 1979, a 29-year-old Oregon man died after swallowing one. Tetrodotoxin works by binding to voltage-gated sodium channels in nerve cells, blocking the flow of sodium ions like a cork in a bottle. This stops nerve impulses, causing paralysis and death by asphyxiation.

The common garter snake (*Thamnophis sirtalis*) is the only known predator that can eat a rough-skinned newt and survive. Many garter snake populations have evolved resistance to tetrodotoxin thanks to genetic changes that alter the shape of the sodium-channel protein, preventing the toxin from binding. These snakes can test a newt’s toxin level by partially swallowing it, then either eating it or letting it go. This predator-prey relationship is a classic example of co-evolution: mutations that give snakes resistance put pressure on newts to produce more toxin, which in turn favors snakes with even stronger resistance—an evolutionary arms race. In some areas, snakes have developed such high resistance that newts cannot keep up. This resistance has evolved independently in at least two garter snake species and at least twice within *T. sirtalis*.

Even resistant animals are not immune to the toxin’s effects; they are usually slowed down. Snakes with some resistance move more slowly after a TTX injection, while less-resistant ones become paralyzed. Newts themselves are not immune to their own toxin—they only have heightened resistance. Each time they release the toxin, they inject themselves with a small amount, which concentrates in certain tissues after passing through cell membranes. To protect themselves, newts have evolved a single amino acid change in their voltage-gated sodium channels, similar to the adaptation seen in pufferfish.