A neurotoxic food chain
info
Format for printing
All of these posts about neurotoxins made me curious about how lethal toxins could evolve in the first place. Sure it makes sense from a defensive stand-point: something eats you; that something gets poisoned/crippled/dead. But, well, you got eaten, so it doesn’t seem like that great of a deal for you. I read a few papers on the subject and found some clues in the model of batrachotoxicity in poison dart frogs and Pitohui birds.
First, plants produce toxins to fend off animals. Second, animals mutate and evolve to resist toxin. Third, larger animal eats resistant animal. This is where some problems are encountered by humans. There’s a nice evolutionary gradient from the plants to the large animals. Direct survival of the plants rests completely on their ability to defend themselves (inability to run away and all). Survival of the animal that eats the plant is generally not so unilateral unless the animal can eat only one type of plant. If that is the case, selective mortality favors resistant mutations. Resistant mutations are not so difficult to come by if the toxin affects a specific binding site. In some bivalve mollusks a mutation in a single amino acid residue leads to a slight change in the sodium channel that saxitoxin affects. There is a clear advantage to resistance; if you are the only animal that can eat a certain plant source then you've got a monopoly on that food source. The chain of mutation can continue if the large animal is dependent enough on the small animal. This is seen with poison dart frogs from Columbia. These frogs consume carpenter ants in the wild that are thought to consume toxic plants. It appears that the evolutionary step from the resistance to a toxin in your diet to its incorporation into your defensive repertoire is not so large. In the end the frogs produce batrachotoxin which works by binding to voltage-gated sodium channels and inhibiting their closure. This leads to irreversible depolarization. I suspect that the homobatrachotoxin of the genus of birds endemic to New Guinea called Pitohui has evolved in the same way. These birds eat beetles that eat a plant…… and on and on.
First, plants produce toxins to fend off animals. Second, animals mutate and evolve to resist toxin. Third, larger animal eats resistant animal. This is where some problems are encountered by humans. There’s a nice evolutionary gradient from the plants to the large animals. Direct survival of the plants rests completely on their ability to defend themselves (inability to run away and all). Survival of the animal that eats the plant is generally not so unilateral unless the animal can eat only one type of plant. If that is the case, selective mortality favors resistant mutations. Resistant mutations are not so difficult to come by if the toxin affects a specific binding site. In some bivalve mollusks a mutation in a single amino acid residue leads to a slight change in the sodium channel that saxitoxin affects. There is a clear advantage to resistance; if you are the only animal that can eat a certain plant source then you've got a monopoly on that food source. The chain of mutation can continue if the large animal is dependent enough on the small animal. This is seen with poison dart frogs from Columbia. These frogs consume carpenter ants in the wild that are thought to consume toxic plants. It appears that the evolutionary step from the resistance to a toxin in your diet to its incorporation into your defensive repertoire is not so large. In the end the frogs produce batrachotoxin which works by binding to voltage-gated sodium channels and inhibiting their closure. This leads to irreversible depolarization. I suspect that the homobatrachotoxin of the genus of birds endemic to New Guinea called Pitohui has evolved in the same way. These birds eat beetles that eat a plant…… and on and on.
Trackback url: http://neurobiology.pharyngula.org/index.php/trackback/3204/RHWNbLl0/