Evolution of Poison

Taken in a broad sense, this question really is no different than asking how teeth or claws might have evolved, and the broad answer is: as the result of cumulative small changes in the genomes of the ancestors of these organisms, as they struggled to survive in environments which included other organisms, some of which were potential predators, some of which were potential competitors for the same food sources, and some of which would have made good eating themselves if they could be persuaded to hold still long enough.It's important to note here that, like any other trait, toxicity cannot be considered independent of context. Just as any advantage confered by teeth or claws depends entirely on the availability of something to bite or scratch, any use of the term 'poisonous' should be considered to implicitly incur an obligation to answer the question: "to whom?" Oxygen is toxic to some bacteria, and carbon dioxide is toxic to animals.For microorganisms, the ability to produce certain chemicals may be considered the equivalent of teeth and claws. They have been conducting research and development in such chemical warfare for several billion years, and so it is not surprising to find that many organisms which employ the use of some type of toxin don't actually produce the substance directly, relying instead on some type of bacteria to do that for them. The Komodo Dragon is a good example; its mouth is a cesspool, teeming with some very agressive bacteria. Just how it is that the Komodo is able to act as host to such lethal guests without succumbing to their effects itself is a question currently being investigated with great interest. In applying the above question to this sort of case, what we are really asking about is the origin of the symbiotic relationship between a toxin-producing microorganism and its host.It's a different question when we ask about how exactly the production of toxins is accomplished (either by microorganisms or by other organisms which do produce their own toxins directly) -- that is: "which genes are involved in the production of such a toxin, and how could the modern versions of those genes be the result of small incremental changes in ancestral forms?" At this point, we'd need to narrow the parameters of the question; we'd need to be asking how the ability to produce a particular toxin might have evolved in a particular organism (with some venomous organisms, such as land snakes, it's going to be a bit more complicated than that, since their venoms tend to be rather complex chemically). As a perusal of the first article linked by kongstad above suggests, this may get a little hairy. Investigating the technical details may look a little too much like biochemistry homework to keep it comfortably within the scope of an informal discussion board like this one, but it's still interesting. I propose that a relevant quote from that article is this:"All of the snake toxin types still possess the bioactivity of the ancestral proteins in at least some of the toxin isoforms".A definition of isoforms is needed here:"Different forms of a protein that may be produced from different genes, or from the same gene by alternative splicing."here's another:"The protein products of different versions of messenger RNA created from the same gene by employing different promoters, which causes transcription to skip certain exons. Since the promoters are tissue-specific, different tissues express different protein products of the same gene."

The poison found in in the granular glands of newts of the family Salamandridae is especially toxic, and was given the name tarichatoxin after its isolation in western newts of the genus Taricha. Tarichatoxin is biochemically identical to the water soluble alkaloid tetrodotoxin (anhydrotetrodotoxin 4-epitetrodotoxin, tetrodonic acid), or TTX, the third most potent non-protein neurotoxin known to exist. Upon entering the blood stream, TTX blocks the sodium channels of excitable membranes, causing paralysis in the nerves and muscles.Tetrodotoxin is found in Japanese pufferfish and in several other poisonous animals including globe fish, sun fish, trigger fish, blue-ringed octopus, frogs of the genus Atelopus, seastars, xantid crabs, horseshoe crabs, numerous marine snails, flatworms, and sea squirts, with more species still being discovered.It is thought that the toxin is acquired through the food chain from TTX-synthesizing bacteria. Through natural selection, pufferfish and other animals possessing TTX took advantage of a single-point mutation in their sodium channel that rendered them immune from the toxin. This enabled them to consume and adapt the poison to their systems without experiencing any ill repercussions.Welcome livingunderworld.org - Hostmonster.comIn other words, for these animals, evolving the ability to use these toxins required only the aquisition of resistance to toxic elements already available in their environments. Many of the sophisticated adaptations we observe (the speed of the cheetah, for example, or the camouflage of stick insects) seem best explained as the results of this sort of 'arms race'. But there are other big questions, such as: "are bacteria of the genus Vibrio really the source of TTX in salamanders; if so, how exactly do the amphibians aquire it; and how exactly do the bacteria produce it?" In my youth, I was (regretably) often willing to injest substances which could easily be regarded as 'poisonous', with the express intent of achieving a similar effect. I now limit my deliberate intake of toxins to caffeine, with the express intent of counteracting a paralysis which, as I get older, seems more and more to be my natural, unmedicated state.