Garter snakes like to eat newts. Newts don't like to be eaten, and to deter snakes from eating them, they have evolved a seriously lethal neurotoxin. This toxin, called tetrodotoxin (TTX), is chemically similar to that found in pufferfish, and a few milligrams is enough to take out a hefty adult human.

But some garter snakes really like newts, and instead of searching for other prey, several species of garter snakes have managed develop resistance to newt neurotoxins.

So how does neurotoxin resistance evolve? A group out of Utah State University, writing in PNAS has used the garter snake - newt evolutionary feud to ask some basic questions in evolutionary genetics:

Are currently adaptive alleles recruited by selection from standing genetic variation within populations, moved through introgression from other populations, or do they arise as novel mutations? Here, we examine the molecular basis of repeated adaptation to the toxin of deadly prey in 3 species of garter snakes (Thamnophis) to determine whether adaptation has evolved through novel mutations, sieving of existing variation, or transmission of beneficial alleles across species.

Where do adaptive genetic variants come from - existing genetic variation, new mutations, or hybridization with related species or populations? In a sense, this issue gets at the question of how evolutionarily malleable species are. When a species is confronted with a new environmental challenge, are there generally beneficial mutants on hand, somewhere in the population, to confront that challenge, or are such 'pre-adaptations' typically rare?

It's unlikely that there is any universally applicable answer to this question, but biologists can get an idea of the lay of the evolutionary landscape by examining many different examples of adaptation.

In the case of garter snakes and newts on the Pacific coast of the United States, it turns out that the resistance mutations in three different species of newt-eating snakes all occur in a gene encoding a membrane-embedded sodium channel that controls electrical impulses in skeletal muscle. But in the different species, the specific mutations in the sodium channel gene are different, meaning that resistance to TTX did not evolve in the common ancestor of present-day garter snake species, nor did it spread through cross-species hybridization. Mutations in the sodium channel, causing resistance to TTX, evolved independently at least three times in different species. In other words, we have yet another example of evolution converging repeatedly on the same solution to an environmental challenge.

The authors sum it up nicely:

The results of this study provide a significant commentary on the convergent acquisition of adaptive alleles in natural populations faced with strong selective pressures. Adaptive changes in the TTX resistance phenotype have a simple genetic basis mediated by a few mutations of major effect. In addition, these amino acid changes occur in a critical locus with strong pleiotropic effects likely to result in significant molecular evolutionary constraints. Taken together, these observations suggest that in situations where a few changes in a gene of major effect are involved, independent evolution may be a common motif. Adaptation via the recruitment of standing variation or hybridization may be more commonly observed in situations where polygenetic changes are required, or where adaptive alleles do not have deleterious pleiotropic effects on fitness and are essentially neutral in the absence of the selective pressure that renders them beneficial.

If there is an obvious evolutionary solution to a given problem, requiring only a few genetic changes of large effect, Nature will use that solution again and again.