In Part 1, we learned about the discovery of crazy toxic newts and their crazy-toxin-resistant prey. I also outlined the basic premise of the “arms race” between the rough skinned newts and garter snakes, explaining how increased toxicity provides selection for increased resistance, which provides selection for increased toxicity, and so on. In this post, I’ll explain how new research (free summary piece here) has filled in the details of this classic tale, then pull back a bit to focus on the major takeaway.
When we left off, Joel McGlothlin of Virginia Tech had identified three mutations that confer tetradotoxin (TTX)-resistance by altering the structure of sodium channels. The first mutation, 1.7, altered the structure of sodium channels along small peripheral nerves (nerves not found in the brain or spinal cord). This mutation is found in all snakes. The second mutation, 1.6, affects larger peripheral nerves and is found in many, but not all snakes. The final mutation, 1.4, affects sodium channels in muscle cells and is found in only five species of snake.
Their next step was to determine when each mutation arose. To do this, McGlothlin’s team analyzed the sodium-channel genes of seventy-eight species of snake along with two lizards (the closest non-snake relatives to snakes), one turtle, and for good measure, a bird. They determined that the mutation to channel 1.7 occurred more than 170 million years ago—before there were snakes or newts! The mutation to 1.6 occurred independently in four snake lineages about 40 millions years ago, which coincides with the evolution of newts (snakes evolved from a group of lizards about 140 million years ago), and the mutation to 1.4 occurred at least five times in five different snake lineages about 12 million years ago.
That's a lot to take in, so let me break it down a bit further. The original resistance mutation arose among the common ancestors of snakes about 170 million years ago. Since there were neither toxic newts nor snakes of any kind at that time, it’s safe to say that this mutation spread and persisted because it conferred some advantage having nothing to do with the evolutionary arms race that rages today. But spread and persist it did, and the trait was passed on to snakes when they evolved about 140 million years ago. Then, for 100 million years or so, snakes evolved on their merry way, all the while carrying a trait for altered type 1.7 sodium channels that would then, by pure happenstance, provide some baseline resistance to TTX-carrying newts when they arrived on the scene about 40–50 million years ago.
Snakes were then able to chow down on the newts not because they magically developed resistance, but because they were already carrying it! Such a good reminder that evolution does not give organisms what they need. Adaptations do not arise because they’d be awfully handy to have. Rather, evolution works with the raw material on hand, and natural selection results in the most advantageous variations present becoming more and more common within a population in a given environment. (I ranted about this in a previous post...well, many previous posts, but here's just one.)
So, snakes were able to eat toxic newts thanks to their pre-existing mutation to channel 1.7. But altered channel 1.7 alone cannot stand up to very high TTX concentrations. Newts that happened to have higher levels of TTX therefore would survive more often than those with lower levels. Some alleles (forms) of the 1.7 mutation, however, were stronger than others, so snakes with greater resistance survived and reproduced more often than those with a weaker form. Over generations, the average toxicity of the newts would increase, and so, too would the average resistance of the snakes. Eventually, the 1.7 mutation became fixed among snakes—meaning that all snakes had the same form of the mutation—which would seem to suggest that snakes reached peak resistance. But then along came a new mutation to sodium channel 1.6 that arose—by chance!—among a few groups of snakes. These snakes could better withstand the bulked up toxicity of the newts. Originally, there were multiple alleles to the 1.6 mutation, just as there was to the 1.7 mutation. As eons pass, a now familiar pattern unfolded: the newts grew more and more toxic, and the strongest, more resistant mutation to the 1.6 channel became fixed among the snakes.
Then what? Well, you get the final mutation arising—again, by chance!—about 12 million years ago that altered the structure of sodium channel 1.4 in muscles. This mutation is "the big one" when it comes go TTX-resistance. Snakes with the 1.4 mutation are able to withstand way highter doses of TTX than are snakes with just the 1.7 and 1.6 mutations. It’s worth nothing that the 1.4 mutation arose only among snakes that had the 1.6 mutation. It likely showed up in other snakes, but without the 1.6 mutation, the advantage was not strong enough, for whatever reason, to spread. (Recall that all snakes have the 1.7 mutation, but only four lineages evolved the 1.6 mutation.) And so, here we are today, with five snake species (including three garter snakes) that each independently evolved extreme resistance to TTX. Each of these species regularly chow down on toxic TTX-baring amphibians that would easily kill most other animals. As with the others, there are multiple alleles for the 1.4 gene, but in this case, the gene has not become fixed. This explains why some snakes are more resistant to TTX than others—it all depends on the 1.4 allele that they have.
I know I've gone into the weeds a little bit with this one, but the details are super cool to us evolution-nerds. To help get us back to the big picture, I’ll quote the lead researcher McGlothlin:
One of the general take home messages of this is that evolution that happens now is building upon millions of years of evolutionary history. Certain pathways that evolution might go down are closed off because the right things didn’t happen in the past, and other pathways are open because the right things did happen.
Of course “right” and “wrong” are only meaningful in retrospect. It’s not that the snake ancestors that evolved the first mutation to channel 1.7 could have thought, “ooh, this is going to be so useful to our ancestors in about 130 million years!” Rather, what McGlothlin is trying to explain is how evolution is contingent. We all carry around the evolutionary baggage of our past. Sometimes, the baggage represents a closed-off path—we humans have lost our tail-growing capabilities but we all inherited a tailbone from our human ancestors. But other times, evolutionary baggage opens a door, as with the snakes. They all inherited a mutation to sodium channel 1.7 that just happened to provide an advantage down the road. So who knows, maybe one day our tailbones will prove they’re good for something other than bruising.
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