The issue of sympatric speciation -- or how to separate species emerge from a single species without geographic isolation -- is a contentious issue in evolutionary biology. How can two species emerge without reproductive isolation of two separate groups? Wouldn't they all just breed together, hiding any new genes in heterozygotes?
Bomblies et al. publishing in PLoS Bio have something interesting to say about that. The use a plant called Arabidopsis thaliana or thale grass to show that the answer might be in genes that regulate the immune response.
Just to get some background, the genes that I am talking about are the genes that allow the animal or plant (yes, plants do have an immune system) to recognize the difference between self and non-self. In humans, these genes are called Major Histocompatibility Genes (MHC). In plants, these genes are called R genes. In particular, one gene involved in immune recognition in the species of plant in this study is called NB-LRR. (Yes, I recognize that things are much more complicated than that, but I am trying to simplify here.)
Now humans and usually thale grass are diploid. (Funky stuff often happens in plants where they can gain extra chromosomes, but we are going to ignore that for the moment.) That means that for each MHC or R gene has two copies in a single individual.
What happens a particular individual inherits two MHC/R genes that are so different that they recognize the individual rather than just pathogens as foreign?
What happens is an autoimmune disease. In human beings, if you have particular MHC genes you are more likely to get autoimmune diseases -- examples include Type 1 Diabetes, Crohn's disease, and vitiligo. In some cases, the incompatibility might be so bad that the individual may not even be viable. They will not survive.
This is the model that Bomblies et al use to investigate immune gene incompatibility in plants. They cross different strains of thale grass, and they observe that 2% of them die from what is called hybrid necrosis.
Hybrid necrosis is when the plant gets sort of a running start at life but then just keels over. (This contrasts Jake-induced plant necrosis where plants die due to lack of watering.) Hybrid necrosis occurs in the absence of any observable pathogen. The researchers show that hybrid necrosis in this case is being caused by two incompatible NB-LRR genes.
The figure below, from the Bomblies paper, shows the range of rather pathetic looking hybrid necrosis phenotypes. On the sides are the two strain that were crossed. In the middle is the resulting rather sad looking plant.
What does this say about sympatric speciation?
Well, let's assume that in a plant species the two R genes diverge in a tiny way, and say one of the R genes mutates making that individual more likely to breed. This is not unreasonable because a heterozygote, an individual who has two different R genes, might recognize a wider number of pathogens. The two R genes are still compatible, but this new heterozygousity allows them to more pathogens making them more reproductively successful.
Now let's say that the progeny of these plants could be heterozygous at the R locus or they could be homozygous -- possess two of one or the other the R gene variants.
As the divergence between the R genes increases over time, there is a point where the two R genes in heterozygotes would no longer be compatible: they would result in hybrid necrosis. At this point, two plants in the same species -- the homozygotes at either end of the genetic spectrum -- would no longer be able to breed together because none of their resulting offspring would be viable.
Two species would have effectively emerged, all without geographic isolation. This is a possible mechanism for sympatric speciation.
(Evolutionary biologists, did I completely butcher that explanation or is that more or less right? Definitely not my area of expertise...)
I was interested in this study because it shows how a tiny gene variant in immune genes can be sufficient to separate two strains. We tend to think of speciation as involving large numbers of genes, and it does in later stages when the forms diverge. The trouble has always been how it starts. Is only one gene necessary to start the process of divergence? Is geographic isolation that would allow large numbers of genes to change necessary? We don't know.
This research suggests that even in cases without geographic isolation, speciation is still possible.
As an interesting side note, the researchers show that under certain environments, in this case lower temperatures, they can rescue the plants that would have otherwise undergone hybrid necrosis. They can save even the incompatible plants by growing them in the right way. This is interesting because it highlights the role of environment in speciation. In some environments, two strains may not be compatible. In others, they might be fine. Particularly, if you consider my example of how this would work above, the presence of a pathogen that makes heterozygotes more successful is necessary to trigger speciation. Just remember, environment matters in evolution.
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1. Isn't A. thaliana a selfer?
2. I don't see how this can work in pure sympatry because the excess divergence between R genes would be prevented by selection against incompatible (ie, infertile) individuals.
I should read the article....
With respect to 1, I think that it is not an obligate selfer. I think it can -- as they say -- swing both ways.
With respect to 2, I see where you are going on the grounds that individuals that cannot breed with a portion of the population would be less reproductively successful. Would it matter if the population was large enough that you could always find a similar mate?
Would it matter if the population was large enough that you could always find a similar mate?
Good question: after all, this may be why we haven't yet selected out stupidity or fugliness:)
You are speaking about a single possible cause of autoimmunity.
I was a scientist some time ago (I hold PhD in physics) so I easily recognize scientific style.
If your blog supposed to be purely scientific, everything is OK.
Regretfully, I do not see any direct help for autoimmunity sufferers.
I am agree with you that MHC genes container may on more risk to be affected by autoimmuniyt but the exact gene which causes the such autoimmune conditions is different may be different from MHC like for the Pigmentation disorder vitiligo a gene NLAP1 is responsible. And same is true for other auto-immune disorders either these may be pigmentation disorder or other.
Where you are disappearing on the foundation that persons that cannot class with a segment of the people would be a lesser amount of reproductively triumphant.