Biochemical Warfare

Coevolution can produce mutually rewarding friendships, but it can just as easily turn species into finely tuned enemies. The constant menace of a predator may drive animals to evolve faster legs or harder shells or better camouflage. In response, their predators are free to evolve faster legs of their own, or stronger jaws or stronger eyes. Predator and prey can thus get locked in a biological version of an arms race, each opponent developing some new adaptation, only to be outstripped by its enemy’s evolution.

This arms race may produce brute strength or speed, but it can also create chemical warfare of exquisite sophistication. One of the best places to see it on display is in the wetlands and forests of the Pacific Northwest. There you can find the rough‑skinned newt, an 8‑inch‑long amphibian with a brilliant orange belly. When one of these newts is attacked, it displays its belly, which a predator would do well to recognize as a warning. If it eats the newt, it will almost certainly die because the newt produces a nerve toxin powerful enough to kill 17 full‑grown humans or 25,000 mice.

Since only a fraction of the poison made by a newt would be enough to kill most of its predators, it seems to be indulging in overkill. But there is one predator that remains a threat to even the most poisonous newts. Edmund Brodie Jr. of the University of Utah and his son Edmund III, a biologist at Indiana University, have discovered that the red‑sided garter snake can eat rough‑skinned newts without dying, thanks to a genetic resistance to the newts’ poison.

In other predators (including other species of garter snakes), the poison blocks certain channels on the surface of nerve cells, jamming their communication and causing a fatal paralysis. But red‑sided garter snakes have evolved nerve channels that cannot be completely blocked by the poison. The snakes may become immobilized for a few hours after they eat a newt, but they recuperate eventually. The menace of garter snakes has driven the evolution of more toxin in the newts, which has driven the evolution of more resistance in the snakes.

This arms race between snakes and newts doesn’t move forward in some kind of simple, species‑wide march. That’s not how evolution works. Instead, the struggle between predator and prey plays out in hundreds of local populations. In places such as the San Francisco Bay area and the northern coast of Oregon, coevolution appears to be running at top speed, creating highly toxic newts and highly resistant snakes. But just as there are coevolutionary hot spots, there are also coevolutionary cold spots in their range. In the Olympic peninsula, for example, some populations of newts make almost no toxins at all, and the snakes that eat them have hardly any resistance.

The Brodies suspect that the unique circumstances of each place are setting coevolution’s course. Evolving resistance to rough‑skinned newts does not come without a price. The more resistant snakes are, it turns out, the slower they crawl. There’s a trade‑off between resistance and speed that the Brodies don’t yet fully understand, but it puts resistant snakes at greater risk of getting attacked by birds and other predators. The coevolutionary cold spots may be places where garter snakes are under heavy attack. On the other hand, the hot spots may represent places where garter snakes depend on the newts because other prey are rarer. Whatever the cause of these hot spots and cold spots, the genes that evolve in each of them spread across the ranges of newt and snake. Sometimes the cold spots will stop the arms race in its tracks, but in other cases the coevolutionary hot spots may drive an entire species to deadly extremes.