A Beautiful Web of Poison Extends A New Strand

I just got back yesterday from the annual meeting of the Society for the Study of Evolution. It took place in a big hotel on the outskirts of Norman, Oklahoma, during a windy heat wave that felt like the Hair Dryer of the Gods. It had been a few years since I had last been to an SSE meeting, and I was struck by how genomic everything has gotten. No matter how obscure the species scientists are studying, they seem to have outrageous heaps of DNA sequence to analyze. A few years ago, they would have been content with a few scraps. Fortunately, SSE hasn’t turned its back on good old natural history. There were lots of fascinating discoveries on offer, about species that I had assumed had been studied to death. My favorite was a talk about the rough-skinned newt, the most ridiculously poisonous animal in America.

The scientific tale of the rough-skinned newt begins five decades ago, with a story about three dead hunters in Oregon. Reportedly, the bodies of the hunters were discovered around a camp fire. They showed no signs of injury, and nothing had been stolen. The only strange thing about the scene was the coffee pot. Curled up inside was a newt.

In the 1960s, a biologist named Butch Brodie got curious about the story. The newt in the coffee pot–known as the rough-skinned newt–has a dull brown back, but when it is disturbed, it bends its head backward like a contortionist to reveal an orange belly as bright as candy corn. Bright colors are common among poisonous animals. It’s a signal that says, in effect, “If you know what’s good for you, you’ll leave me alone.” Brodie wondered if the newts were toxic, too.

Toxic, it turns out, doesn’t do the newts justice. They are little death machines. The newts produce a chemical in their skin called tetrodotoxin, or TTX for short, that’s made by other poisonous animals like pufferfish. Locking onto sodium channels on the surface of neurons, TTX blocks signals in the nervous system, leading to a quick death. In fact, TTX is 10,000 times deadlier than cyanide. While we may never know for sure what killed those three Oregon hunters, we do know that a single rough-skinned newt could have easily produced enough TTX to kill them, and have plenty of poison left over to kill dozens more.

Now, if the whole idea of evolution makes you uneasy, you might react by saying, “That couldn’t possibly have evolved.” Experience has shown that this is not a wise thing to say. Brodie said something different: the most plausible explanation for a ridiculously poisonous animal is that it is locked in a coevolutionary arms race with a ridiculously well-defended predator. Another biologist mentioned to him that he’d seen garter snakes dining on rough-skinned newts, and so Brodie investigated. He discovered that garter snakes in rough-skinned newt territory have evolved peculiar shape to the receptors on their neurons that TTX would normally grab.

The coevolution of newts and snakes became a family business. Brodie’s son, Edmund, grew up catching newts, and today he’s a biologist at the University of Virginia. Father and son and colleagues have discovered that snakes have independently evolved the same mutations to their receptors in some populations, while evolving other mutations with the same effect in other populations. They’ve also found that both newts and snakes pay a cost for their weaponry. The newts put in a lot of energy into making TTX that could be directed to growing and making baby newts. The evolved receptors in garter snakes don’t just protect them from TTX; they also leave the snakes slower than vulnerable snakes. They’ve studied newts and snakes up and down the west coast of North America and found a huge range of TTX potency and resistance. That’s what you’d expect from a coevolutionary process in which local populations are adapting to each other in different environments, with different costs and benefits to escalating the fight.

This story is so irresistible that I’ve written about it twice: first, ten years ago in Evolution: The Triumph of an Idea,, and then in updated form last year in The Tangled Bank. I figured that the Brodies et al had pretty much discovered all there was to know about these creatures. But in Oklahoma, I discovered that they had missed what is arguably the coolest part of the whole story.

Think about it: you’re a female newt, you’ve fended off attackers with a staggering amounts of poison in your skin, and now you want to pass on your genes to your descendants. You lay a heap of eggs in a pond, and what happens? A bunch of pond creatures come rushing in and have a feast of amphibian caviar.

What could you possibly do to ensure at least some of your offspring survived? Well, you have an awful lot of TTX in your system. You have enough of the stuff to give your eggs a parting gift to help them out there in the cruel, predator-infested world. Make your eggs poisonous.

That is exactly what female newts do. In fact, they load their eggs with TTX. To figure out if this poison provided a defense against predators, the Brodies and their students traveled to a group of ponds in central Oregon that are home to thousands of rough-skinned newts apiece. They collected dragonflies and other aquatic predators from the ponds and put them in buckets filled with newt eggs, along with muck from the pond bottoms. The scientists found that almost none of the predators would touch the newt eggs. Since these predators eat plenty of eggs of other species, this result shows that TTX does indeed help the newt eggs survive.

But there was one exception. Caddisfly larvae turned out to relish the newt eggs. In fact, the caddisflies actually grew bigger if they were supplied with newt eggs and pond muck than with pond muck alone. And yet the Brodies and their students estimate that there’s enough TTX in one newt egg to kill somewhere between 500 and 3700 caddisflies.

You know where this is going. At the evolution meeting, one of their students, Brian Gall, described feeding newt skin to caddisflies both from the central Oregon ponds and from ponds elsewhere without newts. The newt-free caddisflies would happily munch on newt skin from which all the TTX was removed. But if there was more than a trace TTX in the skin, they refused to eat. The caddisflies that fed on newt eggs, on the other hand, would eat the most toxic skin Gall could provide.

It appears that the caddisflies have evolved much like the garter snakes. In ponds where rough-skinned newts lived, the caddisflies have evolved defenses against TTX. In fact, Gall reported, the caddisflies appear to put the snakes to shame. Evolved snakes are 34 times more resistant to TTX than vulnerable ones. The caddisflies have increased their resistance 175 times.

It’s not clear whether the caddisflies and the newts are truly co-evolving, however. The Brodies will have to find out whether adding extra TTX to eggs increases their survival in the presence of caddisflies. Another intriguing possibility arises from their discovery that the caddisflies actually harbor some of the TTX they eat in their tissues for weeks after eating the eggs. Perhaps the caddisflies are stealing the poison to protect themselves, as happens in monarch butterflies eating toxic milkweed.

In other words, this wonderfully deadly story isn’t over yet.

[For more information, see this new paper in Can. J. Zool., and Understanding Evolution, an educational web site. Ed Brodie tells much of the story pre-caddisfly in a chapter of the new book, In The Light of Evolution (full disclosure: I wrote a chapter in it, too, which you can read as a pdf here)]

Image: California Herps

11 thoughts on “A Beautiful Web of Poison Extends A New Strand

  1. Incredible picture and great story! As someone who has handled rough-skinned newts on many occasions (they are very common on Vancouver Island), I should point out that they are generally very docile little creatures and release their toxin through their skin only when they are seriously stressed or threatened (such as potentially being boiled inside a coffee pot). They pose little or no danger unless one takes a bite out of them or licks one’s hands after handling them violently.
    I once caught half a dozen on a artificial fly while fly fishing in a small lake and I could have easily hurt myself if I already didn’t know their story and didn’t wash my hands well before eating my sandwich.
    In this picture (http://twitpic.com/5eu0p5) my daughter is petting one in a local natural history center. When I told her about the poison, the 16-year-old interpreter dismissed it as an urban myth – they only taste bitter she said. And that is how people die. I directed her to one of the amphibian field guides sold at the center.

  2. Wow! That is so cool. I’ve been using this as a “textbook” example of coevolution in my classes for years. I love that there is now more to the story. Thanks for the post and the citations!

  3. Really interesting!

    You wrote something above that reminded me of a question I have always meant to ask. Maybe you can help me understand the issue better.

    You said, “Bright colors are common among poisonous animals. It’s a signal that says, in effect, “If you know what’s good for you, you’ll leave me alone.””

    I’ve heard this repeated many times. However, I’ve also heard it often pointed out that animals use bright colors to attract their mates (just like some humans do).

    Don’t these two approaches directly contradict each other?

    Thanks.

    [CZ: Indeed, bright colors are part of sexual displays. But they tend to be on ornaments–a rooster’s comb, or the red spot on a red-winged blackbird. Aposematic colors, as they’re known, tend to cover the whole body. I don’t know if anyone has shown that the same signal serves as a mating signal and an aposematic signal, but it’s conceivable. After all, one signal can have two different meanings for two different species.]

  4. A good story gets even better. I’ll repeat a suggestion I made to an earlier post – the fact that the race isn’t maxed out at highly poisonous/highly poison tolerant everywhere, suggests to me that the race goes in cycles. At some point, the cost becomes too high, and mutants that give up the poison to rely on other survival factors/give up poison tolerance to feed on something else, become favored and reset the race at a zero point for that area.

    Or maybe populations are replaced by nearby ones without the poison/poison tolerance, and the race starts over. Either way, the system has no single stable point of equilibrium.

  5. Last year I was running a course on Asian Security, which involved a slew of guest lecturers from the Security and Defence Studies Centre at our university.

    At one lecture, the first slide the speaker put up was of a rough-skinned newt, to illustrate what he was about to say about arms races.

    If I recall my reading correctly, the term “arms race” began as a metaphor in strategic studies, then started being used by scientists and has now turned back the other way.

  6. Don’t these two approaches directly contradict each other?

    Why should it? A poisonous species would presumably have some means of resisting the toxins it carries in its own body. It wouldn’t be concerned about the poison in a con-specific, so there’s nothing stopping it from viewing the coloration as a sexual signal. Indeed, extra bright coloration could be a signal of improved capacity for manufacturing/collecting the important toxin, and could represent an honest(or dishonest, for that matter) signal of fitness that would serve very well as a sexual signal.

  7. Very interesting. I expect that studying the reason the TTX-resistant snakes are slower may reveal something general about neuron function.

    And while I’m going out on limbs — could the story about the three hunters have been the basis for an X-files episode? If so, it’s a basis far removed. The episode was about swarms of poisonous flying creatures attacking hunters en masse. I know; I really reaching.

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