Convergent adaptations form one of the most striking classes of proof for evolution by natural selection. Radically different species, with common ancestors deep in the past, show near-identical adaptations to similar environments. Convergence can even be seen in species that are separated by vast depths of time, such as icthyosaurs (extinct marine reptiles) and dolphins, which show strikingly similarities in their bodily form, a consequence of adaptation to the environment (water) and their predatory role, based on a common tetrapod anatomy and musculature.
However, most examples of convergent adaptation remain at the level of form or function, rather than the genes involved. It’s possible that the same genes are involved in shaping a dolphin and an icthyosaur, but it’s unlikely we’ll ever know. An exception is the recent discovery of convergent mutations in species of sand lizards with white skins, all of which affect the melacortonin-1 receptor. But in a way, that isn’t too surprising – the melacortonin-1 receptor controls skin colour in these animals, and only a restricted number of molecular changes would give rise to an advantageous white form.
Even more striking is the announcement, shortly to appear in the pages of Current Biology, of identical skin toxins produced in two lineages of frogs, but on the basis of two different genes that diverged during the Cambrian, between 488 and 557 MY ago!
Both lineages of frogs – the Australian Litoria species and the Pipidae (which includes the model species Xenopus laevis) – secrete caerulein, a powerful toxin that induces vomiting, diarrhea and pancreatitis, amongst other things. Strikingly, the two sets of amphibians have very different ecologies and are separated by massive distances – the Australian/Papuan Litoria frogs tend to be terrestrial, whereas Xenopus and its African relatives are strictly aquatic. This means that their toxins are used to ward off very different predators, although the assumption is that in all cases the predators are vertebrates, which are all vulnerable to these toxins.
Researchers in Belgium and Australia, led by Kim Roelants, studied the genome of these frogs, and also looked at the proteins they produced, and discovered that although the caeruleins produced by the two sets of species are identical, they use very different genes to get there.
In the case of Xenopus and its relatives, the caerulein gene evolved through duplication of the cholecystokinin gene (cck); in the case of Litoria, the gene involved was gastrin. Both these genes are present in all vertebrates, but diverged during the Cambrian, and subsequently evolved into a series of genes with different functions in different lineages.
In both cases, gene duplication – when a gene gets mistakenly copied through a genetic accident – provided the raw material on which natural selection could work. With two versions of a gene, one is able to maintain the important function that originally led to its presence, will either evolve randomly (and eventually become a pseudogene, no longer functional) or will accidentally produce a product that is in some other way advantageous to the organism that carries it.
In the case of the cck gene, there were several such duplication events, including two within the lineage that led to Xenopus – there are now three cck genes in Xenopus.
The authors explain this striking case of molecular convergence by the fact that the products of both cck and gastrin genes retained a common structure; this meant they could both function in the frog’s physiology and produce a compound that would repel a wide range of vertebrate predator (by affecting the same physiological processes).
In other words, natural selection was able to use gene duplication to maintain one function, and select another, focusing on the same tiny character, but in two very different genes.