In the arms race with venomous snakes and their victims, several mammals have independently evolved similar defence mechanisms.
Snake venoms work in a variety of different ways; cytotoxins that break down cell walls, Cardiotoxins that stop the heart beating, and hemotoxins that can cause the victim's blood to thicken and clot. Among some of the swiftest and deadliest venoms are the neurotoxins, the toxins that specifically target the nervous system causing paralysis, convulsions, respiratory failure and, in many cases, death.
One of the most common types of neurotoxin is the α-neurotoxin; utilised by a large number snake species including the especially potent venom in the sea snakes and cobras. This family of toxins functions by blocking signals between the nervous system and the muscles. By binding to nicotinic acetylcholine receptors on the surface of the muscle fibres the toxin prevents signals transmitted by the neurotransmitter acetylcholine passing between the nerve ending and the muscle fibre.
Several groups of mammals have managed to evolve resistance to these neurotoxins: the mongoose, hedgehog, and the honey badger. A study conducted by researchers at the University of Minnesota and published in the scientific journal Toxicon demonstrated the chemical bases for this resistance.
By looking at the genome of these species, and focussing on the sequence that was responsible for the production of nicotinic acetylcholine receptors, the researchers were able to identify mutations at two sites which conveyed the resistance.
These mutations were very similar when comparing the hedgehog to the honey badger, yet did not exist in other closely related species, indicating the two species had independently evolved the same solution to surviving the venom.
Interestingly, the domestic pig, whose resistance had been suspected but never experimentally tested before, displayed identical changes to the honey badger at the two sites. Consequently, all three species, the pig, hedgehog and honey badger had convergently evolved; they had independently acquired the same defences against the snake venom.
The function of the mutations at these two sites was to slightly alter the structure of the receptors. While they would still be receptive to the acetylcholine, they prevent the neurotoxin from binding and inhibiting the receptor, allowing the nervous system to remain in control of the muscle.
The mechanism by which α-neurotoxins attack a victim (1) the acetylcholine receptor on the muscle cells, it can bind with acetylcholine to transmit nervous impulses (2) the neurotoxin binds to the receptor, blocking acetylcholine (3) the alternate receptor, changed by mutations in the genome, will still bind to acetylcholine but not the neurotoxin.
The Mongoose on the other hand did not share the same mutations at the two sites of interest, though there were mutations at both sites they were of a different type to that seen in the pig, hedgehog and honey badger. This difference indicates that while a different chemical pathway is used, the functional result is the same; the prevention of the neurotoxin binding to the receptor site.
Examples of convergent evolution such as this are especially interesting as they show that organisms can evolve similar or identical traits all the way down to the genetic level. Whilst convergent evolution has been known about for a long time (similarities in form and behaviour can be seen relatively easily by watching different groups of animals), it has only recently with the invention of modern genetic analysis technologies that discovering examples of genetic convergence has been possible.
Looking into the genome for examples of convergent evolution is especially powerful as it can reveal similarities between species where similarities are not thought to exist, such as between the pig and the honey badger, revealing insights into the evolutionary history of these animals; in this case indicating that the domestic pig has a history of conflict with venomous snakes.