+1 for extending the original question
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Haibao Tang
Does The Urushiol (Poison Ivy) Mutation Predate Humanity?
Today while scratching my poison ivy rash I discovered that humans are the only animals affected by urushiol. So naturally, I want to know why the mutation to produce it exists when it doesn't deter consumption by other animals. Specifically I'd like to know how old this mutation is, if this can be determined, and whether this correlates to the advent of its itchy victims.
If it does predate humanity, I'm curious whether it's good for anything else, though this is a very different question, about which I did find this http://resources.metapress.com/pdf-preview.axd?code=kp835414h8p86007&size=largest
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I would guess that the existence of the biochemical pathway that produces urushiol very likely predates the emergence of Homo sapiens. Urushiols are a family of organic compounds produced in many different plants. We may be acutely aware of this compound (some more than others) because of it's irritant properties - but that doesn't mean that it's only purpose is to be an irritant. I think your question raises a number of different questions with regard to bioinformatics. (1) Urushiol is an irritant, but the precursor to the most irritable form likely has some other purpose. If so, is it a single mutation that allows the irritable form to be produced? If so, how can this mutation be dated? (2) Did the single mutation give rise to the irritant phenotype (potentially a positive selective step) with no negative consequence, such as causing too may off pathway products to be formed? How would this be measured? (3) Or did it arise by gene duplication, and allow off pathway steps to occur without modifying a key pathway component? And how would the timing of this gene duplication be measured bioinformatically? (4) Or if you don't accept that urushiols have any purpose but to irritate humans, and that the pathway for it's production developed solely for this purpose, how does one measure, bioinformatically, how long an entire pathway takes to come into existence?
So I think your question brings up several questions, many of which are bioinformatically complex, and for which little or no specific data exists (yet). To know how old mutations leading to an off pathway effect are, or to development of a whole new pathway, you'd need the sequence of several related organisms (no?). A simpler way to put it might be: what do you think a family of plants can do (in terms of evolution leading to biochemistry) in a million years (about the amount of time humans have been around)? How might you use bioinformatics to show or prove biochemical potential?
This is cool, years after the fact I find a post by my old boss, on one of my favorite topics...
Just for posterity, the question is partially misguided -- genetics is probably not a major driver in the ability to be urushiol-sensitive, however, degree of sensitivity does appear to have genetic components.
How it works: urushiol active ingredients are ~22-carbon molecules, far too small to be detected by the immune system. But they can act as haptens, which means they can non-covalently bind with a host protein, and -- if the hapten-protein combination is just right -- the immune system will misidentify that protein and trigger a response. I don't think the host protein(s) involved are known at this time, or what their phylogenetic distribution is. They are known to exist in all surface epithelia, including skin, lungs, mouth, GI tract.
I see it often claimed in books that only humans are sensitive, and maybe a few other primates. However, urushiol dermatitis research has been carried out in mice, rats, hamsters, and guinea pigs, which all react (check it out on Google Scholar). Vet reports also exist about dogs eating poison ivy, and they react too. On the other hand, deer eat tons of the leaves with no effect. Birds eat the berries too and are fine. So maybe sensitivity is mostly a Euarchontoglires thing, with a few other unlucky animals?
Mutation(s) could conceivably be behind reaction severity in humans, but immunity is a complicated thing -- studies have indicated that sensitivity in parents predicts sensitivity in children; non-sensitives can become sensitive after repeated exposure, and rates seem to vary significantly between Americans and Europeans; and that age has a strong effect on sensitivity, with younger people more likely to be sensitive. Sensitivity can also be reduced through repeat exposure, although I haven't heard of anyone losing sensitivity in this way.
Not that I am an immunologist, but I suspect sensitivity is not related to this protein or that, but is more related to a reactive protein-surface topology, which could exist on multiple proteins. This would also complicate the genetic question.
So you've got a great question, but it may be a long time before it gets answered!
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this is not a clear bioinformatics question but perhaps if you reformulate it as such it can remain open
This is much more of a medical or population genetics question than one pertaining to bioinformatics. Try searching and reading the results returned from a search of PubMed. Maybe WebMD can help.
I was under the impression that genes can be dated to see when the mutation occurred. I know for example that they have been able to determine when the sickle cell gene entered the human population. All references to this seem to be on bioinformatics pages. I am not in any related field, I just had a question that it seems no one has looked at. I don't have access to even determine whether poison ivy and related plants have been sequenced, or whether the urushiol production gene has been identified. Hopefully someone will find this interesting.
Dating of particular mutation is often done using coalescent theory and simulations. This would require assay of this mutation in different human populations. Dig up the literature a bit more to see if you can get a gene or SNP identifier. Poison ivy plant has not been sequenced, and is not relevant here. It is a human mutation that triggers the allergic response.
What is the evidence that only humans are affected by urushiol?
Also, notice that poison ivy and poison oak doesn't grow outside North America, which was populated late after Homo Sapiens was formed.
Wow, you must be kidding! Unfortunaltely, I have a bad sense of humor, so....
Urushiol improves water retention; it is not a defensive mechanism (and wouldn't be very useful for that purpose, since its effects occur long after contact and since those plants are not very interesting to humans).
The fact that it is irritating to humans is likely a consequence of a comparatively aggressive human immune system; i.e., humans are very good at fighting new diseases. The evolutionary reason for why our immune system is so good is probably because we are long-lived, mature late, have few children, and our children require a high investment, so defense against disease becomes evolutionarily more important relative to other species.