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Biomedical Engineering | Polymeric Nanoparticles | Drug Delivery
4 months ago

Does epigenetics play a role in speciation?

I was thinking about how similar neanderthal and our DNA is, and wondered if there were more stark epigenetic differences between us that could explain some of the reduced viability of hybrid offspring.

In any case, it got me wondering if, in general, epigenetic changes like DNA methylation were in part responsible for reproductive isolation and the beginnings of speciation, i.e. differential methylation that gives positive fitness for two different groups in the same species but negative fitness when hybridized could result in less successful crossing between the groups.

I found a paper that I think supports this idea, but I'm not an expert in this field and also don't know how much of an outlier this paper is. Also, even if this happens, I don't know how common it is or how big a role it is thought to play in speciation.

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First off, you are correct in your interpretation of the paper. The authors suggest that speciation may be a result of, as you put it, stark epigenetic differences. You've also presented a likely mechanism. Two different methylation patterns provide a reasonable level of fitness, but anything in between is less fit; as per natural selection, these two populations may continue to proliferate to the point that speciation occurs.

Unfortunately, my background allows me to discuss the biochemical genetics only, so I know as much as you on whether or not the linked paper has standing in the field. However, the paper has received 19 citations in the last two years, and any citing publications appear to take your linked paper at face value.

The more interesting discussion here is your question about epigenetics relating not just to the process of speciation but to the separation between species. And the answer to that question is... maybe.

The first dilemma here is that the definition of a "species" is not entirely stable, in spite of what we're taught in schooling - reproductive isolation and phenotypic differences being the primary two factors. The reason for this instability is the development of DNA sequencing, which has allowed us to explore speciation on a genetic level. Genetic analysis has, for example, suggested that African elephants are, in fact, two different species of elephant.1 Even if we decide to proceed with our pre-genetics definition of species, the question remains. To use your example, there is evidence that neanderthals and H. sapiens interbred as recently as 100,000 years ago.2

There are even questions about the degree to which genetic differences affect speciation. A seminal review in the field says that "the answer is yes, sometimes." A single genetic difference explains 83% phenotypic variation between two species of monkeyflower, but the largest region of variation in Drosophila explains only 11%.3

This entire time, we've been discussing actual sequence differences rather than epigenetics. In that case, does epigenetics play a role in speciation? To my knowledge, there is not much literature dealing with the subject specifically. However, we do have some things to consider. For example, we know that different species can have conserved regions, and we're beginning to realize just how much influence epigenetics has on developmental processes previously attributed to genetics proper. And, as we previously discussed, we believe epigenetics plays a role in at least the initiation of speciation, and that genetics may or may not play as large a role in speciation as previously thought.

So, in conclusion, the answer to your question is... probably.

  1. doi:10.1371/journal.pbio.1000564

  2. doi:10.1038/nature16544

  3. doi:10.1016/S0169-5347(01)02167-X

I love all the comments so far - really cool to think about some of these ideas involving epigenetic inheritance specifically. There is some evidence that imbalance in methylation at certain imprinted genes can reduce hybrid viability, but the extension of these findings in nature is limited, I believe.

If we take a step back from epigenetic inheritance to epigenetic processes, we can talk about histone modifications and DNA methylation, for example. One of the best examples of ongoing reproductive isolation is Prdm9 in mice, which is a histone methyltransferase broadly in charge of altering recombination sites. While divergence at the DNA level has resulted in different Prdm9 alleles at the protein level, the incompatibility takes place at the epigenetic layer (histone modification).

Immunotoxicology and Developmental Toxicology
4 points · 4 months ago

I personally do not think so. Studies of transgenerational inheritance show that the effect of epigenetic marks generally only reliably persists to the F3 generation in mammals and gets weaker and weaker in subsequent generations.

So if you have a metastable allele in which different phenotypes are produced among a genetically identical population, and only the group with better fitness survives, their offspring will inherit some of the epigenetic profile that conferred that advantage, but will lose that advantage in subsequent generations. Assuming that no genetic mutations occurred to confer additional protection, it could very well happen that the group will just die out as the original epigenetic marks fade over the period of germline inheritance.

Biomedical Engineering | Polymeric Nanoparticles | Drug Delivery
Original Poster1 point · 4 months ago

Studies of transgenerational inheritance show that the effect of epigenetic marks generally only reliably persists to the F3 generation in mammals and gets weaker and weaker in subsequent generations.

Is this the case when the mark has a fitness advantage under certain selective pressure, and that pressure persists for the younger generations?

Also, could you give me your expert opinion on the article I linked, whether it applies to my question, and how out-of-left-field it is?

Immunotoxicology and Developmental Toxicology
3 points · 4 months ago

I still think the theory may be a bit reaching in some ways, but if the epigenetic links are specifically geared toward mating and reproductive behaviour as the authors suggest, then it may be more possible. I also like how they bring up genetic assimilation of epigenetic marks in the introduction as another possible mechanism.

The problem with epigenetics research right now is that its a bit too complex to really use it answer every question we have with it right now. We still can't put it in the context of health and disease as a reliable mechanism because of reverse causality. Right now, I'm most convinced of the role of epigenetics in regulating developmental gene expression. For questions outside of development, I don't think we know enough to draw definitive conclusions.

Also, this paper only addresses DNA methylation, which I believe to be generally less impactful on gene regulation than post translational modifications on histones, since for low CpG density promoters, a change in methylation probably won't do anything to change gene expression.

epigenetic profile that conferred that advantage, but will lose that advantage in subsequent generations.

Wouldn't that mean those subsequent generations would die off as well without maintaining the advantage from the previous F1, F2 generations?

Immunotoxicology and Developmental Toxicology
2 points · 4 months ago

That’s what I would think, but the result would differ if that selective pressure went away, such as if they moved to a different place, which is already known the be important for speciation.

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