Meeting Abstract
The rapid evolution of venom toxin genes is often attributed to an arms race between venomous animals and their prey, implying that the trophic role of venom is central to its evolution. However, several species of mammals – including honey badgers, opossums, hedgehogs, and mongooses – regularly prey on venomous snakes and appear to be immune to the toxic effects of their venoms. The molecular basis of venom resistance is complex and is only beginning to be understood. Some toxins are neutralized by proteins that are present in mammalian serum, but these venom-neutralizing factors can only account for resistance to a few kinds of toxins. Other toxins have apparently lost their effect due to rapid adaptive evolution of venom-targeted molecules. Here, we present two examples of rapid adaptive evolution of mammalian genes that are targeted by snake venom toxins. The first involves adaptive changes in a blood coagulation protein – von Willebrand Factor – that may account for the ability of some opossum species to survive envenomation by pitvipers. The second involves convergent evolution of a venom-targeted neuroreceptor – the muscular nicotinic cholinergic receptor – that accounts for the ability of mongooses, hedgehogs, pigs, and honey badgers to survive envenomation by elapids. These examples suggest that molecules involved in venom resistance are also evolving rapidly, and that the role of venom in predator defense may be just as important in venom evolution.
