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Researchers: Basic tenet of evolutionary theory “upended” by new find

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Illustration of Cryptococcus neoformans (stock image). | Credit: (c) Kateryna_Kon / stock.adobe.com
Cryptococcus neoformans (stock image)/© Kateryna_Kon ,Adobe Stock

Looking past the tabloid prose, they say they found that selection can occur at the level of the epigenome:

The field of evolutionary biology has seen its share of spirited debates. But if there’s one principle that virtually every expert in the field agrees on, it’s that natural selection occurs at the level of the genome.

But now, a UC San Francisco-led research team has discovered the first conclusive evidence that selection may also occur at the level of the epigenome — a term that refers to an assortment of chemical “annotations” to the genome that determine whether, when and to what extent genes are activated — and has done so for tens of millions of years. This unprecedented finding subverts the widely accepted notion that over geologic timescales, natural selection acts exclusively on variation in the genome sequence itself.

In a study published Jan. 16, 2020 in the journal Cell, the researchers show that Cryptococcus neoformans — a pathogenic yeast that infects people with weakened immune systems and is responsible for about 20 percent of all HIV/AIDS-related deaths — contains a particular epigenetic “mark” on its DNA sequence, which, based on their lab experiments and statistical models, should have disappeared from the species sometime during the age of the dinosaurs.

University of California – San Francisco, “‘Living fossil’ may upend basic tenet of evolutionary theory: Natural selection’s reach extends beyond genome into epigenome, study suggests.” at ScienceDaily (January 16, 2020)

So what becomes of neo-Darwinism if selection isn’t tied to the all-powerful but accidental gene?

Paper. (paywall)

See also: Epigenetic change: Lamarck, wake up, you’re wanted in the conference room!

Comments
transgenerational epigentic inheritence is possible. It seems to be extremely rare in mammals and (relatively) common in plants. But your questions highlight the porblem for people that want to use this to overthrow mainstream evolutoinary biology. If epigenetic changes are rapid and turnover quickly then they are only noise over evolutionary time-scales, switching back and forth rapidly. If they are stable over many generations then we are back to have a source of heritable information which contributes (or doesn't) to an organisms reporductive sucess. So out ordinary popgen models (with slight modificatoins for epi-mutations) are in play. It's true that we couldn't find the genetic variants responsible for a gene-expression trait that was inherited epigenetically. But we can survey histone and DNA modificatoins with sequencing technology too. We might not be abel to learn precisely what caused the initial production of the epi-allele (but note in the case of the OP we do), but that doesn't seem like a big problem to me. Again, I do think the paper in the OP is really interesting. It's quite a suprise to me that epigenetic modificatoins can be maintained for so long by natural selection, and it's good evidence for how damagin TEs can be.Mimus
January 22, 2020
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Mimus
Even if it turns out a lot of traits are the result of selectoin acting on hertibale variation in epigenetics and not hertibale variation in genetics, I’m not sure it would matter a great deal?
I don't know but I would think at least it would require new models and projections, given that the impact of DNA sequencing itself on phenotype would have been overstated. But I've learned that the safest guess in these matters is that no matter what we find, it's not going to be considered that significant. I had a discussion with Bob O'H last week on that topic. He felt that no matter what new function we might find for non-coding DNA regions that it wouldn't have much significance overall. The science media tries to sell it as something big. Probably the researchers who make discoveries want it to be important. But for biology in general, it doesn't seem to register. I'd imagine that there could be some surprising influences from epigenetic factors and if, for example, we discovered that non-observable environmental pressures (stress, climate) caused changes in gene expression and then those changes were heritable (I'm just hypothesizing) that would mean something more. It's sort of like a learned behavior that is somehow transmitted.
In some cases at least, it seems that the effects on gene expression may persist even after the removal of the inducing agent, and can be passed on, through mitosis, to subsequent cell generations, constituting a heritable, epigenetic change. If such changes occur in germ cells or their precursors, then they may be passed on to subsequent generations. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2781845/
Is that true? Possible? I don't know. Those researchers claim it, but it's hard to assess. But if true, would it mean that virtually invisible, disappeared, factors changed DNA expression from deep history and we'd have no way to discover or trace it? Again, I don't know - I'm just speculating and attempting to understand more.Silver Asiatic
January 22, 2020
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@36 ET
Natural selection is a process of elimination. It doesn’t “act” on anything.
There is some dude out there saying "we are always hallucinating". (Bornagain77, could you please remember us who is that person? You have lots of amazing information and quotes). Maybe "Natural Selection" is an hallucination? Were not we designed to see patterns where there are none?Truthfreedom
January 22, 2020
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Natural selection is a process of elimination. It doesn't "act" on anything.ET
January 22, 2020
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Darwin didn't know about genes, let alone DNA methylation. Selection of epialleles goes back at least to 2002 (https://doi.org/10.1016/S1369-5266(02)00233-9), can happily be modelled by extensions to standard pop-gen models (https://doi.org/10.1016/j.tpb.2011.08.001). Even if it turns out a lot of traits are the result of selectoin acting on hertibale variation in epigenetics and not hertibale variation in genetics, I'm not sure it would matter a great deal?Mimus
January 21, 2020
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Mimus
FWIW, the selectability of epialleles is not a crazy new idea.
Of course not. "We knew about this for a long time." The Theory predicted it. I think Darwin knew about it, if I'm not mistaken.Silver Asiatic
January 21, 2020
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That's some typo... ;)ET
January 21, 2020
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I think it's fairly obvious from context that there's a typo there, read it as "cannot" (or cannot always) map directly.Mimus
January 21, 2020
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Mimus:
It’s true that DNA sequence alone can map directly to phenotype...
That is far from true. When the human genome was mapped the scientists didn't find anything that linked the genome to "humanness". It is true the DNA controls and influences development. But that is about it.ET
January 21, 2020
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This is really pretty garbled, but you seem to be confusing ancestry and phenotypic similarity. DNA sequences will tell us how closely related species are, and I don't see how epigenetics (as in DNA methylation) changses. It's true that DNA sequence alone can map directly to phenotype, but that's basic 1930s quantitative genetics (invented by Fisher and other evolutionary biologists) and nothing in DNA methylation alters this.
will guess that the very same people who claimed that epigenetics had virtually no impact at all on the development of organisms Which totally real people are these? FWIW, the selectability of epialleles is not a crazy new idea. It is amazing that negative selection on epialleles can maintain methylation for so long though. Just goes to how strongly selected transposon silencing is (almost as if they are mostly junk DNA...).
Mimus
January 21, 2020
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Mimus Ancestry will be assumed because of sequence similarity (although I assume common design from the creation of life) but the question would be how closely related the organisms are and how they diverged. Confusion about ancestry seems to be only one of the problems with the inclusion of epigenetic mechanisms into evolutionary explanations though. In this case, similar DNA can show different morphology. So, estimating how similar various organisms are based on DNA similarity alone would give inaccurate results. In two organisms with similar DNA sequencing, if epigenetic factors were present at some point in history for one and then lost, then new features developed in that one and not in the other. How does that get traced? But that's only one problem and I can see how it would be dismissed simply under the assumption that sequence similarity necessarily means descent by modification. A bigger problem arises when projecting backwards (which, instead of predictions forward seems to be all that evolutionary theory can do), there at least four variables to contend with: Random mutations, Random external environmental effects (food supply, competitors, weather, etc) random epigenetic factors and non-random selection for fitness. How does the addition of another random factor that may or may not be selected for and cannot be found in the historical record, affect whatever evolutionary predictions or explanations that can be made? There is some attempt to calculate the effect of negative mutations to DNA sequences but what about the negative effect of epigenetic factors? In this case, the researchers do not know the effect of various epigenetic mechanisms on the development of other species.
"But now the big question is 'Is this happening outside of this exceptional circumstance, and if so, how do we find it?'"
So again, the theory supposedly explains relatedness on the basis of sequence similarity but whether morphological changes occur because of mutations to DNA or because of random epigenetic mechanisms is unknown. I would think this should tell us something about the "certainty" of evolutionary claims prior to this new awareness (of the selectability of epigenetics) but I will guess that the very same people who claimed that epigenetics had virtually no impact at all on the development of organisms and that all changes were based in changes to DNA sequencing alone, will have no problem with findings that "upend" that notion.Silver Asiatic
January 21, 2020
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@16 Pater Kimbridge
TRUTHFREEDOM asked: “– If there is not design – How can the ‘appearance of design’ exist?” How is it possible to be similar to something that does not exist?
Pater Kimbridge replied:
If I see a mirage in the desert that has the appearance of water, how can there not be water?
Appearance is a relational concept. Something is an 'appearance' when it has a real counterpart (desert mirage= appearance / real water= real). According to Evolution, design is an 'appearance'. If there is 'appearance' of design, it is because there is real design. We know design is real, and we know it because we humans design things. If design is real --- materialism is false (materialism states that design is an illusion). Design is real --- materialism is false. Materialism is false.Truthfreedom
January 21, 2020
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Sure... but SA says
If changes in the phenotype are independent of DNA sequences, then we can’t use sequence similarity alone to make accurate inferences about ancestry.
DNA sequence makes in clear the neotenic Axolotl are not distinct from the metamorphosing ones.Mimus
January 20, 2020
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Neoteny- The Axolotl, is an organism that was once thought to be two different species. Without environmental iodine it never completes its metamorphosis. Yet it reaches sexual maturity and can reproduce before that major change.ET
January 20, 2020
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My key point is that it adds another random variable, making it more difficult to trace lineage
How? I honestly don't see what point you are trying to make.Mimus
January 20, 2020
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EG
Comparison of the genome over time would still be a good indication of ancestry.
That could be the case, I'm actually not sure how it would work. I was considering a scenario where an epigenetic factor emerged in the history of an organism, causing variation in gene expressions and then the development of new features. Then the factor was lost for various reasons, unknown to us today. I think this paper indicates that the researchers are struggling to understand the history of methylation in this organism over time, from what they would have expected (it would be randomly lost in 130 years) and what they eventually found. The selective advantage they assigned to it was in the prevention of transposons, which would end up limiting changes to the genome (and restricting the potential for beneficial mutations). My key point is that it adds another random variable, making it more difficult to trace lineage. But I haven't studied this closely enough to know either way what it really means. Epigenetic signals could simply be treated like any other environmental factor, I suppose. Not sure about that.Silver Asiatic
January 20, 2020
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SA
I wasn’t clear on that. I meant epigenetic influences or factors may cause changes to the phenotype.
Yes, that is my understanding as well.
If changes in the phenotype are independent of DNA sequences, then we can’t use sequence similarity alone to make accurate inferences about ancestry.
But they aren’t independent of DNA sequences. They are just different expressions of the same gene. If the expression changes because the environment changes, the new expression must be either neutral, beneficial or slightly deleterious for it to survive long term. Comparison of the genome over time would still be a good indication of ancestry.
Epigenetic factors which can change the phenotype, add another random variable to evolution.
And a source of heritable variation is a requirement of evolution.Ed George
January 20, 2020
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Ed George
It is my understanding that epigenetic changes contribute to changes in phenotype with no change to the genotype. There is no “may” involved.
I wasn't clear on that. I meant epigenetic influences or factors may cause changes to the phenotype.
How so? Let’s assume that gene A is expressed as phenotype P1 under environmental condition E1, and as P2 under environmental condition E2. If E1 persists for many generations and P1 imparts increased fitness then the gene frequency will increase in the population. If it has lower fitness then it will decrease.
I think the problem would be if E1 was present at one time, but then was lost somewhere in the history of the organism. As such, we cannot trace it. If changes in the phenotype are independent of DNA sequences, then we can't use sequence similarity alone to make accurate inferences about ancestry. We would have to know what kind of epigenetic factors were at work and what effect they had on gene expression over the development of the organism. It makes the idea that evolutionary theory could actually predict the development of a species, or even give a step-by-step gradual picture of the development in the past, even more impossible. Epigenetic factors which can change the phenotype, add another random variable to evolution.. It cannot be as simple as claiming that a new feature emerged because a species had to move geographically or find new food sources or face competition.Silver Asiatic
January 20, 2020
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Acartia Eddie:
It is my understanding that epigenetic changes contribute to changes in phenotype with no change to the genotype.
From Wikipedia on genotype:
The genotype is the part of the genetic makeup of a cell, and therefore of any individual, which determines one of its characteristics (phenotype).
DNA methylation is an epigenetic mechanism that can modify the function of genes and affect gene expression. That, in turn, determines one (or more) characteristics.ET
January 20, 2020
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SA
Epigenetic changes may contribute to changes in phenotypes with no change to the genotype.
It is my understanding that epigenetic changes contribute to changes in phenotype with no change to the genotype. There is no "may" involved. Please correct me if I am wrong.
This is a problem for the inference of ancestry and descent.
How so? Let's assume that gene A is expressed as phenotype P1 under environmental condition E1, and as P2 under environmental condition E2. If E1 persists for many generations and P1 imparts increased fitness then the gene frequency will increase in the population. If it has lower fitness then it will decrease. I think that it is reasonable to predict that if one of the phenotypic expressions was deleterious and the environmental conditions were such that this phenotypic expression was present for many successive generations, that the frequency of this gene might dramatically decline or even disappear. It would be interesting to see if this is the case.Ed George
January 20, 2020
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Epigenetic changes may contribute to changes in phenotypes with no change to the genotype. This is a problem for the inference of ancestry and descent.Silver Asiatic
January 20, 2020
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Upon investigating the crime scene, I determined that it gives the appearance of a man who was attacked by a gryphon.Silver Asiatic
January 20, 2020
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Acartia Eddie:
The phenotype is the result of the genome and the environment.
That is the untestable claim, anyway. However there are geneticists and developmental biologists who disagree.
What we are learning through epigenics research is how the environment and the genome interact to produce the phenotype.
What we have learned via developmental biology is that we do NOT know what determines phenotype. All we know is that genomes and environments influence and control development. But influencing and controlling are not the same as determining. Assembly lines also influence and control what is being manufactured. But they do not determine it.ET
January 20, 2020
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TRUTHFREEDOM asked: "– If there is not design – How can the ‘appearance of design’ exist?" If I see a mirage in the desert that has the appearance of water, how can there not be water? If I see a large man coming toward me in a dark alley, and I am afraid he will harm me, how can he not harm me? If I have an opinion about something, how can there be so many people who have a different opinion? If I am hunting deer and I shoot at a partially obscured shape that sort of reminds me of a deer, how can it not be a deer? If I see a termite mound that resembles a medieval cathedral, how can it not be a cathedral? If the Sun is round and yellow, and a grapefruit is round and yellow, how can the Sun not taste like a grapefruit?Pater Kimbridge
January 20, 2020
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@13 Bornagain77:
“Darwinism provided an explanation for the appearance of design, and argued that there is no Designer — or, if you will, the designer is natural selection..."
Let's examine this gem, atheist evolutionist materialists (not you Bornagain77!) :) - If there is not design - How can the 'appearance of design' exist? How is it possible to be similar to something that does not exist?Truthfreedom
January 19, 2020
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.
the lifeblood of Darwinian evolution is deception
...and often the avoidance of physical evidence, prediction, and history.. Hey Ed, Sev, an irreducibly complex symbol system was predicted by John von Neumann to be the fundamental material condition of an autonomous open-ended self-replicator. That prediction was later confirmed by experiment (Crick, Watson, Brenner, Zamecnik, Hoagland, Nirenberg, etc), and as it turns out, such symbol systems are uniquely identifiable by their physical embodiment, which was further confirmed by Pattee and others -- even being described as a necessary multi-referent language structure required at the origin of Life.. Here is the question for you: Is the gene system an irreducibly complex system of symbols, or not?Upright BiPed
January 19, 2020
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Ed George claims that "The phenotype is the result of the genome and the environment." That claim is false. "Many scientists have pointed out that the relationship between the genome and the organism — the genotype-phenotype mapping — cannot be reduced to a genetic program encoded in DNA sequences.
Not Junk After All—Conclusion - August 29, 2013 Excerpt: Many scientists have pointed out that the relationship between the genome and the organism — the genotype-phenotype mapping — cannot be reduced to a genetic program encoded in DNA sequences. Atlan and Koppel wrote in 1990 that advances in artificial intelligence showed that cellular operations are not controlled by a linear sequence of instructions in DNA but by a “distributed multilayer network” [150]. According to Denton and his co-workers, protein folding appears to involve formal causes that transcend material mechanisms [151], and according to Sternberg this is even more evident at higher levels of the genotype-phenotype mapping [152] https://uncommondescent.com/junk-dna/open-mike-cornell-obi-conference-chapter-11-not-junk-after-all-conclusion/ With a Startling Candor, Oxford Scientist Admits a Gaping Hole in Evolutionary Theory - November 2011 Excerpt: As of now, we have no good theory of how to read [genetic] networks, how to model them mathematically or how one network meshes with another; worse, we have no obvious experimental lines of investigation for studying these areas. There is a great deal for systems biology to do in order to produce a full explanation of how genotypes generate phenotypes,,, http://www.evolutionnews.org/2011/11/with_a_startling_candor_oxford052821.html
In fact, the reductive materialism of Darwinian evolution is at a complete loss to explain how the biological form of any particular organism may possibly be generated by mutations to DNA:
Darwinism vs Biological Form - video https://www.youtube.com/watch?v=JyNzNPgjM4w
As Stephen Meyer explains in the following video, 'you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan.'
‘Now one more problem as far as the generation of information. It turns out that you don’t only need information to build genes and proteins, it turns out to build Body-Plans you need higher levels of information; Higher order assembly instructions. DNA codes for the building of proteins, but proteins must be arranged into distinctive circuitry to form distinctive cell types. Cell types have to be arranged into tissues. Tissues have to be arranged into organs. Organs and tissues must be specifically arranged to generate whole new Body-Plans, distinctive arrangements of those body parts. We now know that DNA alone is not responsible for those higher orders of organization. DNA codes for proteins, but by itself it does not insure that proteins, cell types, tissues, organs, will all be arranged in the body-plan. And what that means is that the Body-Plan morphogenesis, as it is called, depends upon information that is not encoded on DNA. Which means you can mutate DNA indefinitely. 80 million years, 100 million years, til the cows come home. It doesn’t matter, because in the best case you are just going to find a new protein some place out there in that vast combinatorial sequence space. You are not, by mutating DNA alone, going to generate higher order structures that are necessary to building a body plan. So what we can conclude from that is that the neo-Darwinian mechanism is grossly inadequate to explain the origin of information necessary to build new genes and proteins, and it is also grossly inadequate to explain the origination of novel biological form.’ - Stephen Meyer - Functional Proteins and Information for Body Plans – video – 5:55 minute mark https://youtu.be/hs4y4XLGQ-Y?t=354
Ed George also claims that, "The consequence of selection has not been altered. It changes allele frequency." Yet the claim that selection "changes allele frequency" is found to be negligible to non-existent. And thus Ed George's claim here to is also found to be, for all intents and purposes, false.
The waiting time problem in a model hominin population – 2015 Sep 17 John Sanford, Wesley Brewer, Franzine Smith, and John Baumgardner Excerpt: The program Mendel’s Accountant realistically simulates the mutation/selection process,,, Given optimal settings, what is the longest nucleotide string that can arise within a reasonable waiting time within a hominin population of 10,000? Arguably, the waiting time for the fixation of a “string-of-one” is by itself problematic (Table 2). Waiting a minimum of 1.5 million years (realistically, much longer), for a single point mutation is not timely adaptation in the face of any type of pressing evolutionary challenge. This is especially problematic when we consider that it is estimated that it only took six million years for the chimp and human genomes to diverge by over 5 % [1]. This represents at least 75 million nucleotide changes in the human lineage, many of which must encode new information. While fixing one point mutation is problematic, our simulations show that the fixation of two co-dependent mutations is extremely problematic – requiring at least 84 million years (Table 2). This is ten-fold longer than the estimated time required for ape-to-man evolution. In this light, we suggest that a string of two specific mutations is a reasonable upper limit, in terms of the longest string length that is likely to evolve within a hominin population (at least in a way that is either timely or meaningful). Certainly the creation and fixation of a string of three (requiring at least 380 million years) would be extremely untimely (and trivial in effect), in terms of the evolution of modern man. It is widely thought that a larger population size can eliminate the waiting time problem. If that were true, then the waiting time problem would only be meaningful within small populations. While our simulations show that larger populations do help reduce waiting time, we see that the benefit of larger population size produces rapidly diminishing returns (Table 4 and Fig. 4). When we increase the hominin population from 10,000 to 1 million (our current upper limit for these types of experiments), the waiting time for creating a string of five is only reduced from two billion to 482 million years. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4573302/ “Darwinism provided an explanation for the appearance of design, and argued that there is no Designer — or, if you will, the designer is natural selection. If that’s out of the way — if that (natural selection) just does not explain the evidence — then the flip side of that is, well, things appear designed because they are designed.” Richard Sternberg – Living Waters documentary Whale Evolution vs. Population Genetics – Richard Sternberg and Paul Nelson – (excerpt from Living Waters video) https://www.youtube.com/watch?v=0csd3M4bc0Q
It would nice if Ed George would apologize for his false claims and stopped repeating them. But alas, the lifeblood of Darwinian evolution is deception. It simply can't survive without it.bornagain77
January 19, 2020
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@ PW That’s talk text for you :pAaronS1978
January 19, 2020
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Looking past the tabloid prose, they say they found that selection can occur at the level of the epigenome:
Selection acts at the level of the phenotype. The phenotype is the result of the genome and the environment. What we are learning through epigenics research is how the environment and the genome interact to produce the phenotype. The consequence of selection has not been altered. It changes allele frequency. If the epigenetics affect on the gene results in a phenotype that produces more offspring, that gene will increase in the population. If it resulted in a phenotype that produced fewer offspring then that gene would decrease in the population.Ed George
January 19, 2020
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The problem epigenetics presents to Darwinism is that it demonstrates organisms shaping themselves to the environment somehow, rather than the environment shaping organisms via differential survival rates. So the plan is to zoom out to a lower resolution and declare that that is where natural selection rules. Not a good plan, necessarily, but it is a plan.jstanley01
January 19, 2020
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