The word “epigenetics” once meant simply “development”—that is, the way the genome worked itself into an organism through the production and regulation of proteins and absorption of food and materials from the outside, and the turning of some genes on and others off in different tissues. Now, however, the term means roughly “forms of inheritance that rest on modification of the DNA sequence,” and by “DNA sequence” I mean the sequence of four bases (A, G, C, and T) that constitutes the DNA code.
We now realize, though, that some DNA bases can be modified, and in an inherited way, in a manner that can affect the development, behavior, or structure of an organism. Such modification often takes place via DNA methylation, in which some of those four bases acquire methyl groups, thereby changing how the DNA functions.
Such methylation, as you’ll see by reading the Wikipedia link above, is important in organismal development—something we’ve realized only in recent decades. For example, there is differential “imprinting” of DNA via differential methylation in male versus female parents, and this results in the DNA in the zygote doing different things depending on whether it came from mother or father (organisms have paired chromosomes, getting one from each parent). This has led to speculations about the evolution of differential imprinting resulting from different interests of mother and father in how and which zygotes develop.
Methylation is also important in silencing the X chromosomes of female mammals that have two X chromosomes. This silencing equalizes the gene dosage between XX females and XY males (Y chromosomes barely have any genes), so normal development usually means keeping the dose of X-linked genes (and hence the amount of proteins they make) the same in both sexes.
Anyway, that kind of epigenetics is itself based on the DNA code. That is, the A, C, T and G sequences, and the environment in they find themselves, are “programmed” by natural selection to add or remove methyl groups from other parts of the DNA. Such adaptive epigenetic programming must perforce rest on the sequence of DNA bases, because methylation of the DNA is not inherited in a stable way. In imprinting, for instance, those bases that are methylated differently between the sexes are “reset” in the offspring: the methylation vanishes and is re-constituted before reproduction by whatever sex the embryo happens to be. That reconstitution is programmed in the DNA code itself. Methylated bases in DNA don’t usually get passed on from one generation to the next. There are two important points to add.
First, as I said, if methylation is itself an adaptation produced by natural selection, it ultimately must rest on changes in the sequence of unmethylated A, C, T, and G bases in the DNA. Only unmethylated bases are stably inherited, and evolution demands stable inheritance. There must be something about the DNA sequence that controls its own methylation. (Note that some methylations can last for several generations, though that’s not common.) For a population to change over time and acquire adaptations (or features that evolve through nonadaptive processes like genetic drift), whatever types of replicators that are inherited must remain unchanged, with of course the exception of mutations in the DNA code. But if the DNA code changed unpredictably back and forth each generation, natural selection and evolution wouldn’t work.
Second, there are also epigenetic changes that are induced not by the DNA sequence but by the environment. Temperature, starvation, and other environmental factors can cause methylation of the DNA as well. The thing is, though, that such changes, because they’re rarely passed on to future generations, cannot serve as the basis of evolutionary change. Such changes constitute true Lamarckian inheritance, i.e., the inheritance of acquired characteristics.
And lots of studies show us that Lamarckian inheritance doesn’t operate. Changes that are induced by the environment, or the organism’s “striving,” can’t somehow get incorported into the DNA. An athlete, for example, doesn’t produce kids with bigger muscles. And after millennia of circumcision, Jewish boys are still obstinately born with foreskins, giving my readers plenty to argue about.
Further, genetic analysis of adaptations that have arisen in evolution (like differences between closely related species of stickleback fish), invariably shows that they rest in changes in the base sequence of DNA (if that kind of genetic resolution is possible). Those changes can be in either “coding” sequences (that moiety of DNA that makes proteins), or “regulatory” sequences (those bits of DNA that regulate the expression of coding genes). There is, frankly, not a scintilla of evidence that adaptations of organisms rests on epigenetic DNA changes produced solely by the environment.
My conclusion: if epigenetic changes are involved in an evolutionary adaptation, they must be coded for in the DNA rather than acquired from the environment alone.
Nevertheless, there is a vocal subset of biologists who see the “Lamarckian” form of epigenetics as of great importance in evolution: a neglected area that is truly non-neo-Darwinian. This claim rests solely on a few studies showing that epigenetic change in DNA induced by the environment can sometimes be passed on for several generations. But there’s no evidence that this has produced any adaptive features of organisms. The subset of biologists that trumpet “nongenetic” epigenetics as an important but neglected part of evolution—evidence that the modern theory of evolution is wrong or woefully incomplete—are latter-day Kuhnians who seek to forge a new paradigm, a paradigm that rests on shaky pillars.
After all, you don’t get famous in biology by showing once again that neo-Darwinism is right (even though it happens to be!). Epigenetic-mongers of the “Lamarckian” stripe (there’s also a sub-breed involving a process called “genetic assimilation,” which can occur but for which there’s little evidence in nature) are wannabee Heisenbergs. (The Wikipedia article on “genetic assimilation”, at the link above, is a very good explanation of the process, and must have been written by an expert. But note that it adds that “It has not been proven that genetic assimilation occurs in natural evolution, but it is difficult to rule it out from having at least a minor role, and research continues into the question.”)
I write about epigenetics at length because I think we need to understand the claim that discoveries in epigenetics show that modern evolutionary theory is either wrong or incomplete. This claim, which is wrong, often rests on a confusion between the adaptive methylation of DNA that is itself coded for by the DNA, and evolved by natural selection, and the nonadaptive methylation of DNA that occurs by effects of the environment. Adaptive, genetically based epigenesis is a relatively new finding—and an important one, but it’s a finding that fits comfortably within the existing evolutionary paradigm. Only “Lamarckian” epigenesis, in which environmental changes somehow become permanent and inherited adaptations, would pose a severe challenge to neo-Darwinism. And we have no examples of that.
Yet this very possibility is touted in a new Nature News piece by Sujata Gupta, “Epigenetics posited as important for evolutionary success.” The claim in this piece is that recent work on invasive species shows that epigenetic modification is not only helping species invade new habitats, but also in a “Lamarckian” manner:
“There are a lot of different ways for invasive species to do well in novel environments and I think epigenetics is one of those ways,” says Christina Richards, an evolutionary ecologist at the University of South Florida in Tampa.
Although biomedical researchers have been investigating the links between epigenetics and human health for some time, evolutionary biologists are just beginning to take up the subject. Richards, who helped to organize a special symposium on ecological epigenetics at a meeting of the Society for Integrative and Comparative Biology (SICB) in San Francisco this month, says that the field has the potential to revolutionize the study of evolutionary biology.
Well, a lot of far-fetched stuff has the theoretical potential to revolutionize the study of evolutionary biology, including the possibility that the DNA of any species is transcribed only when there’s a plant within 100 miles. What’s important is whether there are data to support that revolutionizing. And in this case, there don’t seem to be. Gupta cites two examples of things that supposedly portend a revolution, one of them suggesting a Lamarckian role in epigenetic evolution. Here’s the first data:
Even so, there are hints that epigenetic diversity could be helping invasive species to thrive. For instance, Andrea Liebl, a fifth-year doctoral candidate at the University of South Florida, studies house sparrows (Passer domesticus) in Kenya, which, as descendants from a single group, have very little genetic diversity. But when Liebl combed the genomes of the birds to look for parts that had methyl groups attached — a key epigenetic marker — she found a high level of variability across populations.
Now this is a meeting report, and apparently hasn’t been published, but what is presented here gives me no confidence that epigenetics plays any role in invasion, nor has anything to do with any feature of these sparrows. This seems to be—the description is unclear—simply a correlation of population differences with DNA methylation differences, not a demonstration that methylation caused the population differences or is somehow involved in “invasibility”. The methylation differences could be produced by the different environments of different populations, and have nothing to do with adaptation—or anything else.
Further, it’s erroneous to imply that only a few invading individuals make the descendant population immune to evolution because it lacks genetic variability. A single fertilized female, for example, carries fully half of the heritable genetic variation of the population from which she came. That fertilized female carries fewer forms of genes than does her population, but those variants that are present are there in high frequencies (this is because a single fertilized female has four genomes, so each variant gene has a frequency of at least 25% in the next generation.) Thus, showing that a group was founded by a few individuals does not mean that it couldn’t subsequently evolve, or that environmentally-acquired methylation must have been important.
Further, even if a group was genetically homogeneous—a group of clones—it could still invade if it’s simply a better competitor than the species already there. Competitive success isn’t always based on evolution after invasion, but simply—as in the cane toad in Australia and Hawaii—on features of the invader that evolved before it invaded, and on evolved features of the residents that make them susceptible to the invader. That’s all well known ecological dogma, and the accepted explanation for why species on isolated islands are often displaced by invaders. I suspect that if all cane toads were genetically identical, they’d still have been successful invaders in Hawaii and Australia. The local fauna simply isn’t used to them! And they’re poisonous!
Here’s the second bit of evidence that Gupta uses to make the case for an important revision of evolutionary theory:
Similarly, in the invasive plant Japanese knotweed (Fallopia japonica), Richards found that genetically identical plants — knotweed reproduces clonally — have different leaf shapes and grow to different heights depending on where they live. Like the sparrows, the knotweeds exhibited high epigenetic diversity. Cristina Ledón-Rettig, a molecular biologist at North Carolina State University in Raleigh, who also helped organize the symposium, says that mapping the level of epigenetic modification may reveal “whether a population is going to tank or survive”.
Here we have a clonal population showing different methylation patterns in different habitats. They also have different phenotypes in different habitats. There is no evidence cited by Gupta that the former causes the latter. Thus such a correlation shows very little.
We’ve long known that clonal plants can assume different growth patterns in different habitats. That may often be because of evolved and adaptive plasticity (if you’re a plant near a tree, start climbing it to get support and sunlight). Alternatively, the patterns may simply reflect nonadaptive developmental responses to the environment. There is no evidence from Gupta’s summary statement that a). the invading knotweed was genetically homogeneous (the study described could have been an experimental one using clones); b). the methylation had anything to do with the different phenotypes in different environments; or c). the epigenetic differences can be inherited from one generation to the next—a prerequisite for “non-Darwinian” epigenetic evolution. Note that the emphasis on clonality, and on genetic homogeneity in the sparrows, is supposed to suggest that the supposedly adaptive methylation patterns were not evolved via changes in the DNA sequence, but produced by the environment and somehow inherited. It’s as if the authors see a necessity for Lamarckian epigenesis because there’s not much variation in the organisms’ DNA sequences.
Gupta talked to me for an hour the other day, and I explained the problems with this idea as best I could, including the many experiments showing that adaptations are based on changes in DNA sequence. She ignored all that. The only caveat that appeared in her piece was this:
Some critics aren’t ready to accept the links between epigenetics and invasive species. Jerry Coyne, an evolutionary geneticist at the University of Chicago in Illinois, says their success can be explained by well-established evolutionary theories. Sometimes a species moves into an unoccupied niche, and sometimes a small amount of genetic diversity goes a long way. “It doesn’t have to have a lot of variation to evolve,” he says. “We have perfectly good other reasons, which are based on more solid premises, on why invasive species succeed.”
Well, there I am again as a cranky old defender of neo-Darwinism. I thought my counterarguments, most of which were omitted, were convincing, or at least worth mentioning, but do you think that Gupta is going to let go of an exciting “non-Darwinian” idea just because of a grumpy biologist like me? No way! She concludes her piece on a revolutionary and upbeat note: Darwinism revolutionized! Much of what we know is wrong!
But with the cost of gene sequencing dropping, symposium organizers predict that research into ecological epigenetics is poised to take off. There could be several powerful studies coming out that show “how gene expression changes if the environment changes”, says Aaron Schrey, a population geneticist at Armstrong Atlantic State University in Savannah, Georgia.
It’s as if I said nothing at all: that adding my critique was merely a journalistic ploy to give a formal nod to the “other side.” Well, maybe ecological epigenetics is poised to take off, but I doubt that, with the data presented, it will revolutionize the field. There are formidable theoretical and empirical problems with the idea that acquired epigenetic markers are important features in adaptation. But of course I’ll keep my mind open in case some are found.
As I said, evolved epigenetic changes based on evolution of the DNA sequence may well play important roles in evolution—roles that we don’t yet appreciate. But I would bet a lot of dosh that we won’t find Lamarckian epigenetics, or even genetic assimilation, playing large roles. The enthusiasm expressed by Gupta and the researchers seems largely unjustified.
I emphasize again that I didn’t go to this meeting, and I don’t think the relevant work has yet been published, so Gupta may not have properly represented the results. But she certainly misrepresented, or at least failed to explain, the underlying biology and theory. Either way, it’s a gross failure of scientific journalism.
Science journalists love new findings that promise to overthrow existing paradigms (we don’t see headlines saying “Still another case of natural selection described!”), but they often fail as real journalists in such breathless pieces. It’s often because they don’t understand the science, or have to leave out important details. Either way, Gupta’s article, if read by people who don’t know about epigenetics, does the field a disservice.
This wouldn’t bother me so much if it wasn’t another of those tiresome claims that modern evolutionary theory is drastically wrong or incomplete because of some recently-discovered phenomenon. I heard the same claims when evo-devo surfaced, and while that area has found some exciting stuff, like the conservatism of Hox genes, it hasn’t changed our underlying view of how evolution works. I predict that in the coming few years we’re also going to hear similar Kuhnian claims about epigenetics. And I predict that findings in that area will also fit comfortably within modern evolutionary theory.
Although I’m a skeptic, and seen as a diehard supporter of neo-Darwinism, I think that an objective observer would agree that that that current paradigm is working pretty well. I haven’t yet heard the guns and shouts of revolutionaries on the horizon.
Jerry, you are on the side of the angels here (so to speak). In an online population genetics theory text that I update, I have an Exercise that I ask students about that makes the analogy between an epigenetic modification and a mutation that has a very high rate of reversion, perhaps once every 3 generations. To keep such a “mutation” in the genome you need natural selection constantly working, with a high selection coefficient. Otherwise the “mutation” reverts, leaving the genome unchanged. The folks who are hollering about long-term evolutionary change being caused by epigenetics are not taking this into account.
It <is possible that an epigenetic modification would create conditions for a subsequent modification of the actual DNA sequence that would stabilize it — along the lines of “genetic assimilation”.
One minor point: epigenetic change is “Lamarckian” rather than Lamarckian — Lamarck himself envisaged a response to use and disuse (or to an environmental effect) that was not random but was preferentially adaptive. Epigenetic changes are random with respect to their fitness effect so they are “Lamackian” but not Lamarckian.
Kindly ignore the typos in the above.
you make a good point Joe. But I think few minor clarifications could me made. First, Lamarck explicitly rejected the direct effect of the environment upon the organisms (except in the “lowest” organisms that originated through spontaneous generation). According to his evolutionary theory, changed conditions made organisms to change their habits through the use and disuse of parts, and this caused the adaptive change. No random variation involved as you say.
Epigenetic changes could be adaptively induced by the environment in the sense that some epigenetic machinery evolved by NS and fixed genetically in the DNA sequence could target the environmental signal to a change in the chromatin. A way to regulate DNA expression epigenetically through chromatin modifications (DNA base methulation and histone modifications).
You are right about Lamarck — he envisaged change by use and disuse, not by direct environmental effects.
You are wrong about “adaptively induced by the environment” — unless the genome has somehow adapted itself to the epigenetic changes, by a genetic assimilation effect. Epigenetic changes such as methylation do not seem to be preferentially adaptive, they are more likely to be maladaptive.
Excellent, lucid, cogent, compelling arguments as always! Why do so many people (scientists and journalists alike) seem to think that epigenetics somehow overturns classical (or real) genetics? Or seem to want it to. It highlights some kind of negative reaction to the findings of genetics research and the way they are portrayed (perhaps in too deterministic a way).
(For a very like-minded view on epigenetics, especially in the field of psychiatry and behaviour, see: The Trouble with Epigenetics:
http://www.wiringthebrain.com/2013/01/the-trouble-with-epigenetics-part-1.html )
Some of these people are, perhaps, so desirous of being in the forefront of a paradigm shift that they toss the natural caution that a good scientist/writer should have in assessing ‘new’ ideas. As my training boss in surgery was wont to tell us:’Do not be the first to embrace the new, nor the last to cling to the old.’ New concepts deserve rigorous testing, and after same, many – if not most – are found wanting.
A wonderful article! There was one point that I didn’t understand though, and I’m hoping that someone here might explain it to me.
A single fertilized female, for example, carries fully half of the heritable genetic variation of a population.
By “population”, does Jerry mean the population that the fertilised female descended from? If so, I can’t see why this would be the case. Anyone care to explain that to this (fascinated-by-evolution) layman?
It is surprising that Gupta did not pick up on the necessity for stable inheritance as one of the essential components of natural selection and adaptation – that there must be at least a statistical resemblance between parents and offspring that is independent of the environment. Of course, I am always skeptical of any pop-science article that contains the phrase “evolutionary success.”
I really don’t see the “puffery” here. I wouldn’t argue that epigenetics will force a revolution in evolutionary biology, but there are a number of reasons to think that epigenetics may be important in the process of adaptation. These data come primarily from plants, which seem to be more prone to epigenetic inheritance than the few animals that have beens studied (this is likely due to the fact that plant germ cells are derived late in ontogeny, after weeks or years of growth, and the fact that epigenetic resetting during meiosis is less complete than in mammals).
A key point is that these studies are in their infancy, and we need much more research before we can say that epigenetic phenomena do or do not play an important role in adaptation. Again, the work in plants in particular demands that these hypotheses be taken seriously. We do know that (1) methylation variation can be inherited in the absence of DNA sequence variation, (2) that many ecologically relevant environmental stresses induce methylation variation, and (3) that methylation variation translates into fitness related phenotypic variation. The key now is to test for each one of these phenomena in the same system under ecologically meaningful conditions.
I think point three is important in so far as it is rarely addressed in general criticisms, certainly if plasticity in expression patterns are adaptive and regulated by the environment.
I would also note that an epigenetic change does not need to be stable for many generations in order to influence evolutionary trajectories. This is because epigenetic mechanisms may underlie many instances of phenotypic plasticity and maternal effects. The modeling literature gives us good reason to believe that plasticity and maternal effects can indeed influence the trajectory of genetic evolution.
The claim Jerry is making, which is the same as Dawkins’ take on the matter, is that adaptation requires the stable inheritance of replicators. Epigenetic changes could be adaptive if coded for by the (stably inherited) DNA code itself. This would be the case even if the epigenetic changes were programmed to be contingent – “only methylate this base if…”. This is why Jerry agrees that “evolved epigenetic changes based on evolution of the DNA sequence may well [later be found to] play important roles in evolution.”
But epigenetic potentials that aren’t coded for simply don’t have the longevity required to effect significant adaptive change. (They can’t be selected for any more if they aren’t present two or three generations later!) They can of course still “influence evolutionary trajectories” (anything can, including asteroids) but that’s not saying they can produce adaptations.
I think you are right; Jerry does seem to agree on my point about epigenetic changes that underlie adaptive plasticity. This is a really interesting avenue of research, as the mechanisms of plasticity have generally been black boxed.
I would argue that we still don’t know enough about the stability of epigenetic changes to make the general claim that they do not persist long enough to form the substrate for selection and adaptation. We need more experimental work, particularly in realistic environments. What we do know suggests that this work really needs to be done. See, for example, the studies on epigenetic recombinant inbred lines in Arabidopsis.
Reblogged this on Mark Solock Blog.
IIRC, epigenetic changes may have played significant roles in evolution by creating conditions that made certain mutations more or less advantageous. For example, after a bacteria has been exposed to a stimulus it will begin to overexpress the relevant receptors and its progeny will also overexpress these receptors for many generations. This may have helped develop hormone-receptor systems, by increasing the significance of the development of a trait to produce the stimulus.
Yes, but mustn’t there be instructions in the stable genome to overexpress the “relevant” receptors – and not make any old change? Isn’t methylation in this case an “adaptive” trait produced in the usual way? Perhaps it is analogous to bacteria becoming hypermutable or showing gene amplification to stress in general.
Its epigenetic in that it doesn’t involve a sequence change not (I believe) in that it results from a methylation. In this case, a bacteria with identical genome and environment would be different based on its parents environment.
The initial expression and “inherited” expressions are certainly results of genes though.
I was at SICB and can report I saw nothing presented that deviates from the norm. It turns out population genetic theory still does an excellent job. But hey adding more jargon and fluffy stories will get you a nature paper!
Surely, that is epigenesis, not epigenetics?
I fully agree that methylation is just one of the things that DNA does, and unlikely to be more significant for evolution than the well-known mechanisms of control sequences, repressors etc. When I learned about genetics and development as an undergrad I was also doing mathematics courses including mathematical logic and theory of computation, and they looked pretty much equivalent (such that once I understood how the basics worked – like a frickin’ Turing machine – I did not want to clutter my mind with the details).
Consider this potential mechanism of non-DNA and hence ‘epigenetic’ inheritance:
Spotted Hyenas (Crocuta crocuta) are well known to have ‘masculinized’ females that (unusual for Carnivora) are larger and more aggressive than males, and also have penis-like external genitalia through which they copulate (ouch!) and give birth (OUCH!!).
OK, maybe that’s all written in their DNA and evolved through allelic natural selection. But maybe it’s not; consider the possibility that it’s an effect of an excess of testosterone (or whatever!) during development, and if they were at lower levels the female would develop ‘normal’ (carnivore-typical) female genitalia etc. But one of the effects of developing in the steroidal pressure-cooker of a butch female spotted hyena is that the female offspring continues to produce high levels of testosterone throughout life, whereas in a male it’s more strictly regulated or buffered or whatever (males are just normal, for hyenas).
So, it doesn’t have to start with a heritable change in DNA: the elevated testosterone in females might originally have been produced in a somatic tumour or injected by a crazed extraterrestrial physiologist, but could be somatically inherited and, if positively selected, would eventually affect every female of the species. It would alter the conditions under which every gene was being selected down through the history of the species, without ever having been caused by a genetic change.
Ê possibile? It would be more interesting than methylation, imho.
http://cdn.memegenerator.net/instances/400x/33265952.jpg
“evolved epigenetic changes based on evolution of the DNA sequence may well play important roles in evolution—roles that we don’t yet appreciate.”
It occurs to me that successfully invasive species might (might) have more epigenetic variations available to them because of their DNA, and that less frequently successful invasive species have less epigenitc variation available to them. Thus a frequently successful at being invasive species would exhibit more phenotypical variation even though they do not have a great deal of genetic variation. It occurs to me though that the eventual changes in the DNA due to mutations, duplications, deletions, and recombinations, might produce phenotypes different from the epigenetically-induced phenotypes that enabled their ancestors to survive in the new environment.
I am having a hard time reconciling this post with the observation that a fetus and its developing germline is epigenetically vulnerable to environmental influences, as is the case with prenatal exposure to the potent endocrine disruptor diethylstilbestrol (DES); and a growing number of studies demonstrate somatic and germline impacts of other substances including other several endocrine disrupting chemicals. If a mammalian fetus and its germline are epigenetically susceptible to noxious compounds such as DES, permanently (or at least for multiple generations) affecting gene expression, is this irrelevant to our understanding of evolutionary biology? Help me, so confused.
Jane —
You exaggerate. The few effects documented are pathological and attenuate to invisibility after 3 generations.
See ‘DES’ on Wikipedia. However, these chemicals do provide good examples of how long-term epigenetic effects are poorly docucmented even under the eyes of aggressive medical researchers.
Thanks for the tip.
W.Benson
Pardon me, W.Benson, for finding your response unclear. Are you saying that endocrine disruptors such as DES do indeed have heritable epigenetic impacts, but that these impacts are minor (tell that to a DES daughter), and fade out over several generations, so are therefore irrelevant to the understanding of evolutionary biology? Are you not evading the issue of germline environmental vulnerability?
This post is over my head. I’ll have to stick to the kittehs.
As a non-scientist even I can see the problem with this “evidence” and “theory.” If the cloned plant with different leaves had actually undergone a heritable change, wouldn’t it just be a matter of cloning it and growing it in the original plant’s environment to prove the change was permanent? Or at least look for changes in the DNA of the naughty bits, where the only changes that matter would be.
My own field got invaded by a species of “thinkers” who tried to overturn the “paradigm” by calling the old farts old farts. Some of them made good points supported with good evidence. Others were just crackpots interested more in making a splash (and getting tenure) than in making a real contribution.
Jewish boys are still obstinately born with foreskins…
Now that you’ve finished reading the Bible, did Jesus come with one?
Apparently
And at the end of eight days, when he was circumcised, he was called Jesus, the name given by the angel before he was conceived in the womb. Luke 2:21
Though medieval Christians decided he must have regrown his foreskin when he got back to heaven, to restore his perfection.
Thanks! No mention of who the mohle was? (After the big deal about the wise men, you’d think the mohle might get passing reference.
Successful mohles must keep their identities secret…
/@
And then:
Some critics aren’t ready to accept the links between epigenetics and invasive species.
How in the hell can you even write such a sentence when the claim hasn’t even been thru peer review?
*sigh* I’m in love. Again.
Reblogged this on Naive Scientist.
The methylation of C residues in DNA, if transmitted in the germ line, may not last many generations. However, it predisposes the C to mutate to T, which henceforth will persist unless it confers a character that is negatively selected. Thus, in principle, a point mutation initially deemed epigenetic can become genetic. For more please see chapter 18 of “Evolutionary Bioinformatics” (Springer, New York, 2011).
Well in vertebrates it’s not just any C but a CG. Anyway this type of deamination explains why CpG islands are rare in gene bodies. They do exist and are observed hotspots for mutation. Most of this work is being carried out in cancer research, but like someone else alluded to, how many ecology and pop gen papers are in to bisulfite sequencing?
Until I went to a talk about the methylation in monozygotic twins it puzzled me that some identical twins appeared identical yet others did not.
If I understood, it depends on how soon the ferilised egg splits. Early meant different methylations could happen in the now two clumps. Later meant that the twins shared many such changes and so would be more likely to appear identical.
Soooo, you may already have seen epigenetics in action!
“how gene expression changes if the environment changes”,
Enzyme activity changes too when the environment changes. Gene expression and enzyme activity are good examples of phenotypic plasticity – phenotypic plasticity is a perfectly heritable trait and can fully be described in standard population genetics models / quantitative genetics.
Totally agree…
Thanks for the detailed synopsis 🙂
Reblogged this on Tropical Bioinformatics and commented:
Some people say that epigenetics are going to change completly the field of evolutionary biology. I think those are overreactions to cool words and reality will be that “findings in that area will also fit comfortably within modern evolutionary theory.”
Excellent job with the epigenetics discussion! And I am in complete empathy and accord with you on the frustration one gets when seeing science journalists take a misunderstood idea and run with it (sometimes due to intentional misrepresentation by the researchers or their institution’s media office or, more frequently, just through a misunderstanding on the part of the journalist). Good curmudgeoning!
And speaking of your role as a curmudgeon, I attended some talk at a conference this weekend on the free will debate and found my inner narrator asking myself, WWJT (What Would Jerry Think)? As a biologist, this conference was way out of my field so I didn’t follow everything. I think the main thing I learned from the experience was a bit about the different presentation styles of philosophers, psychologists, and neurologists. And boy, are there some differences!
Read through the whole article and all the comments but maybe I missed something: aren’t there well-regarded studies proving epigenetic inheritance? Namely: http://www.the-scientist.com/?articles.view/articleNo/33699/title/Inherited-Resistance-to-Cocaine/
Also the Swedish human studies haven’t been addressed either, and supposedly that data is pretty clean from what I’ve heard. Am definitely not an expert though so am curious what I’m missing.
Ok this post from Kevin Mitchell largely addressed my questions:
http://www.wiringthebrain.com/2013/01/the-trouble-with-epigenetics-part-2.html
which were not really brought up here.
Unstable transmutation is still transmutation. Now if by evolution you mean “teleology”, than stable inheritance is required. Strictly speaking, however, a completely random process would still be evolution.
Reblogged this on Bridgewater Society.