Sunday, April 12, 2009
Venom Varieties
On pages 153-154 Carroll discusses potassium channel blocking venoms in organisms from 4 different phyla. How can these different venoms with such different compositions have evolved into these separate phyla of organisms to serve the same purpose? In what way does this phenomenon connect the organisms and tie them together in terms of their separate evolutions? If these organisms share the same means of getting food to survive and reproduce, how can you account for the differences that separated them into their phyla?
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These different poisonous venom that block potassium channels from a sea anemone, a scorpion, a marine cone shell snail, and a black mamba evolved through time through natural selection. Carroll states that “given sufficient time, identical or equivalent mutations will arise repeatedly by chance, and their fate (preservation or elimination) will be determined by the conditions of selection upon the traits they affect (Carroll 155).” Carroll’s discussion of the ultraviolet-sensing and violet-sensing species of birds from different orders further explains how different organisms evolve differently to result in similar evolutionary changes. He states that “when similar forces converge, similar results emerge (Carroll 154).” The violet-sensing and UV-sensing capabilities correlate with a particular amino acid at position 90 in the SWS opsin. Birds with a serine amino acid are tuned to violet, while birds with a cysteine are tuned to UV. The single mutation at position 268 from A to T will occur in roughly 750 million offsprings. Owever, given the number of offsprings every year and time, a serine-to-cystein switch will arise once every 750 years. When regarding the long evolutionary time, it is likely that random mutations occur multiple times and repeat itself to be selective advantages. These random mutations that occur throughout evolutionary time can happen in many different species, and these 4 different phyla that have venom that block potassium channels were proved to be advantageous in their survival, so natural selection preserved the gene and prevented it from becoming fossilized.
ReplyDeleteThey are connected in that all of these organisms from different phyla had mutations by chance that gave the species a venom that blocked potassium channels crucial for the nerve and muscle functions, and this venom gave these organisms a selective advantage in their survival and reproduction of future generations, therefore preserving this selective advantage. Sea anemones have small vesicles filled with toxins—actinoporins—an inner filament and an external sensory hair. When the hair is touched, cell explosion is mechanically triggered and injects a dose of poison in the flesh of the aggressor or prey. The poison paralyzes the prey, which is then moved by the tentacles to the gastrovascular cavity for digestion. Actinoporins have been reported as highly toxic to fish and crustaceans, which may be the natural prey of sea anemones. In addition to their role in predation, it has been suggested that actinoporins could act, when released in water, as repellents against potential predators. Scorpions, black mambas, and marine cone shell snails also use their venom for protection against predators and use it to paralyze their prey during predation. These toxins are also important in that they are used to treat autoimmune diseases in humans. There was a report describing the improvement of symptoms in a patient with multiple sclerosis following a scorpion sting. The venom contained a peptide that blocked a certain potassium channel necessary for the self-attacking T-cells to survive. By blocking the channel, the treatment causes immobility in the T-cells. With no way of survival, the destructive T-cells die off, allowing other white blood cells to fight disease and infection. After this discovery, several other toxins were tested and sea anemone toxins were modified for treatment and marine cone shell snail venoms are also show great promise as a source of a new, medically important substance.
http://www.scorpionfacts.info/venom.php
http://www.newuniversity.org/main/article?slug=sea_anemone_venom_can
http://en.wikipedia.org/wiki/Cone_snail#Harpoon_and_venoms
http://www.newuniversity.org/main/article?slug=sea_anemone_venom_can
The general answer to this question is independent convergence, but you asked specifically why this type of venom was created. We have seen that with similar situations of different species, similar solutions are found because given enough time many of the same mutations will occur, and since the situations are the same, the filter of selection is the same. This will cause the same traits to be filtered through and be retained by an organism. The main question is then, why has the specific type of potassium blocking venom arisen in each species? There are three main types of venom, hemotoxic venom, neurotoxic venom, and cytotoxic venom. Hemotoxic venom affects blood cells; neurotoxic venom, which is the type described by Carroll, damages the brain and central nervous system; and cytotoxic venom damages the local site where it entered. Within these categories there are many different methods that the venom can fulfill their specific tasks, one of the neurotoxic methods would be to block potassium channels, for example.
ReplyDeleteTo solve this problem, a wise thing would be to look at the purpose of the venom. It is obviously either for self defense or for predation. The effects of blocking potassium channels occur rather quickly. Paralysis sets in very quickly after blocking potassium channels. There are many ways for a toxin to kill an organism, but this method might be one of the quickest and most effective method for a predator. It's much more beneficial for a predator to paralyze its prey quickly. After all, it would be useless to kill its prey if its prey has ran far out of range by the time it is dead. Looking at this it seems like this could be one of the most effective means of predation, which answers the question as to why it evolved independently in many different species. Given enough time and a given amount of mutations, a resulting species will retain the most beneficial of those mutations who are beneficial and play a role in the survival of the species. Using this logic, neurotoxic venom must have either been one of two possibilities. It was either the only type of venom that the species were able to slowly develop through mutations, or it fit the circumstances of the different species better than any other types of venom that might have slowly developed through various mutations. To better clarify this “second possibility”, I will give a theoretical example. An example of this situation would be the garter snake, through multiple mutations, developing cytotoxic venom, then when the proper mutations came along to develop neurotoxic venom, it retained these mutations because the neurotoxic venom served its predatory needs more suitably. Then, will relaxed selection on the cytotoxic venom, its genes for cytotoxic venom became fossilized as its presence had no affect on the survival of the snake.
Finally, to address the issue of phyla, species are not divided into phyla based on their source of nutrition. The issue of phylogenic divisions is a completely different idea. Taxonomists used to divide species based on things like mode of nutrition, diet, physiological traits and other observable features After the discovery of DNA, however, taxonomists now rely on this feature to classify organisms, and it has led to many reforms in the phylogenic trees of organisms. Different organisms with the same type of venom might have similar DNA for this specific trait of venom, but the rest of their code may be very different. This is the entire point of independent convergence. Two species that are not closely related can develop very similar features if they are presented with the same “problems”.
http://en.wikipedia.org/wiki/Neurotoxin
http://www.venomous.com/venom.html
The neurotoxins in the venom of the Black Mamba are specifically known as dendrotoxins. The dendrotoxins affects the injected individual by binding to the nodes of Ranvier of motor neurons where they block the potassium channels. Specifically, as basic proteins with a positive charge, dendrotoxin interact with negatively-charged amino acids in the pore of the channels and cause them to close, thus increasing duration of action potentials and the amount of neurotransmitter, i.e. acetylcholine, released in to the synapse.
ReplyDeleteThe phenomenon seen with the structurally different, yet similar functioning neurotoxins in venoms of a sea anemone, scorpion, and cone shell may be an act of convergent evolution as caused by similar prey, predators, or environmental stressors. It could also be a result of a divergence and evolution from a shared ocean-dwelling ancestor. This ancestor was perhaps naturally selected due to its slightly more poisonous secretions, which developed into an effective means of boosting survival. From this "original" venom, the expression of the genes that resulted in the production of the production underwent a genetic mutation, perhaps a point mutation during replication or transcription. An insertion or deletion of one to three nucleotides can result in the addition or absence of certain amino acids to the final protein product. These changes on the genetic to protein level may have resulted in subtle changes in genetic coding; but the resulting product, even with different amino acids, may have been able ot main the same conformation as the original potassium channel blocking venom.
http://www.kingsnake.com/toxinology/snake_neurotoxins.htmlhttp://en.wikipedia.org/wiki/Dendrotoxin