Epigenetics Rules!

_{January 1, 2016

Intelligent Design}

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New news summary out at Phys.Org about ant colonies and their castes. Seems as if this is all being controlled via epigenetic means.

This is not good news if you’re a population geneticist: you know, phenotype changes because of changed allele frequencies (unless, of course, it doesn’t; and then you call it “phenotypic plasticity.” There’s nothing in life that a label can’t explain!!). Well, I guess not.

A snippet:

In the new findings, an interdisciplinary research team led by senior author Shelley Berger, PhD, from the Perelman School of Medicine at the University of Pennsylvania, in collaboration with teams led by Juergen Liebig from Arizona State University and Danny Reinberg from New York University, found that caste-specific foraging behavior can be directly altered, by changing the balance of epigenetic chemicals called acetyl groups attached to histone protein complexes, around which DNA strands are wrapped in a cell nucleus. . . .

“The results suggest that behavioral malleability in ants, and likely other animals, may be regulated in an epigenetic manner via histone modification,” said lead author Daniel F. Simola, PhD, a postdoctoral researcher in the Penn Department of Cell and Developmental Biology. Simola is co-lead author with Riley Graham, a doctoral student in the Berger lab.

Merry Christmas and Happy New Year to all!

Comments

Jonas Crump- We don't know what produces the phenotype. DNA/ genes influence development but do not determine what is developing.Virgil Cain_{January 7, 2016
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PaV: What you wrote is the ‘traditional’ way of viewing things, consistent with the Modern Synthesis." I appreciate your patience. But when you say "There’s a whole lot going on nowadays.", are you not simply saying that we have a better understanding of how the environment interacts with DNA to produce the phenotype we see? I agree, the straight Mendelian genetics (punit square, and all that) is not as black and white as previously thought. But didn't Fisher suggest this 80 years ago? From what I have read, epigenetics just adds more noise (variability) to the system. But, ultimately, changes in allele frequencies still rules the day.Jonas Crump_{January 6, 2016
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Virgil: Not to mock wd400, but I'm sure he would tell you that they know all about these things, and have known it for a long time. But, somehow, they can't construct a phylogenetic tree.PaV_{January 6, 2016
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Jonas: There's a whole lot going on nowadays. What you wrote is the 'traditional' way of viewing things, consistent with the Modern Synthesis. It would be hard to recite all the ways things have changed. The turn of the new millenium has brought fantastic changes in biology labs and techniques. I would recommend you go first to Wikipedia, and then start searching around some of the referenced works.PaV_{January 6, 2016
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PaV: "The question is (and in a certain sense ‘answered’ by wd400) is this: what controls the ‘expression’ (regulation, if you like) of DNA. We now see that, contrary to earlier thinking, it’s not all controlled via strict Mendelian inheritance." But what "earlier thinking" are you talking about? It has been several decades since I was at university (more than I would like to admit), but even in those dark ages we were taught that the phenotype was the result of the interaction of DNA and the environment. Isn't that exactly what epigenetics is? And changes in allele frequencies will change the phenotypes that are possible. Am I missing something?Jonas Crump_{January 6, 2016
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Even with DNA without transcription and translation, including all that is required for that, you have nor proteins, no life. And there isn't any evidence that, DNA and proteins, determines what type of organism will develop.Virgil Cain_{January 6, 2016
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Jonas: Without DNA, you have no proteins---and life, of course, would be impossible. The question is (and in a certain sense 'answered' by wd400) is this: what controls the 'expression' (regulation, if you like) of DNA. We now see that, contrary to earlier thinking, it's not all controlled via strict Mendelian inheritance. Well, how did such a system come about? By mutations? IOW, there is layer upon layer of complexity being found in the cell when scientists peer more closely at it. Remember, in Darwin's time the cell was considered a blob--think of an chicken egg, but much smaller (just drawing an analogy here. The model is: more fit individuals, fixation of DNA, and, given enough time and change via variation and fixation, new species. But now we see fitness being 'directly correlated' to environment, and not via variation, fitness increase and fixation. The inadequacies of pop. gen./modern synthesis are only further heightened by these new discoveries of complexity.PaV_{January 6, 2016
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Mung, "Evolution" and "fitness" of course have meanings (change in heritable traits and the expected number of offspring respectively). Unfortunately, the more technical meanings of epigenetics are now pretty much dead. For the most part it's now indistinguishable form "gene expression".wd400_{January 6, 2016
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This is just all wishful thinking and misunderstanding PaV. Though I have to say "ENCODE undermines pop. gen" is one of my favorites..wd400_{January 6, 2016
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PaV, I understand that. But doesn't it ultimately come back to the DNA? And, if it does, isn't it still prone to NS, genetic drift etc.?Jonas Crump_{January 6, 2016
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Jonas: That's how it was understood 'traditionally.' 'Modern' epigentics involves lncRNA, siRNA, etc, as well as chemical markers. Genotype was supposed to equal phenotype (outside of cell differentiation), but now we see just how 'plastic' the phenotype can be, influenced by many other factors than DNA. It's a whole new world.PaV_{January 6, 2016
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No one understands epigenetics because the term itself is equivocal. It's like trying to understand evolution. Or fitness.Mung_{January 6, 2016
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Maybe I don't understand epigenetics, but doesn't it boil down to genes being expressed in differt ways due to environmental cues? If this is true, then we have understood this for a long time. The sex of turtles is dependent on the temperature during incubation. All clown fish are born male and only the largest most aggressive one in a group becomes female (so much for Finding Nemo). But these are still the results of DNA. Changes in allele frequency will still change phenotypic expression.Jonas Crump_{January 6, 2016
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wd400:
Histone deacetylases and histone acetyltransferases. Or the many hundreds of genes that control the expression of those gene products? You really have to understand these topics before you can dismiss them.
What I'm dismissing is pop. gen.'s insistence that this is all controlled via neutral drift, or mutations and selection. To some extent, this is all very likely true---but ONLY to some extent. That's the difference. The import of 'modern' epigenetics is the strictly environmental component and its inheritability (which is Lamarkian in character). ENCODE undermines pop. gen., by and large. It's time to move on. Shapiro's NGE is the 'wave of the future.' And it points towards ID, and away from today's mainstream pop. gen. The kids you're teaching will be the ones who will lead the way to the future. And, BTW, you made no mention of siRNAs. Now that's really nasty for pop. gen.PaV_{January 6, 2016
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we’d only need histone acetylation agents.
Like. Maybe... Histone deacetylases and histone acetyltransferases. Or the many hundreds of genes that control the expression of those gene products? You really have to understand these topics before you can dismiss them.wd400_{January 5, 2016
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wd400:
What on earth do you think the infinite allele model is? It has ntohing to do with the germline-soma split.
I guess I need to spoon-feed everything. Without the germline-soma split, the idea that 'all' of inheritance is to be found in the DNA of the germline would not have become entrenched, nor would it have led to Fisher and Wright's view of things. Admittedly, they didn't know any better. The fact that the germline is not, in fact, completely cut-off from the soma--something which is very much highlighted by 'modern' epigenetics---overthrows one of the central theses of pop. gen., and thus weakens it further. The "infinite allele" model is just a short-hand for pop. gen., formed as it is by this model. This is part of what Provine was railing against. Here's two articles you should look at: from Evolution and News, and from Nature. One remark that is made in these articles is that it appears that histone acetylation is what controls expression. This would be a blow to the lac operon thinking of Monod which pervades pop. gen. We wouldn't need "alleles" showing up, and then changing: we'd only need histone acetylation agents. As I stated above: epigenetic rules!PaV_{January 5, 2016
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Isn’t it obvious, based on the paper we have in front of us, and the discussion that has taken place, that there are cellular processes of regulation which control other cellular processes, which in turn, have phenotypic consequences, all of which has nothing to do with the inheritance of DNA; and, further, are not passed down via DNA
No. I misunderstood you comment only because the correct reading turns it into a complete non-sequitur. I've already explained that as clearly as I can. What on earth do you think the infinite allele model is? It has ntohing to do with the germline-soma split.wd400_{January 5, 2016
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wd400: You've displayed an inability to understand what is clearly being said on many occasion, but now this:
Do you really think that anyone claims that cell-biology within an organism has much to do with changing allele frequencies within that organism.
How can you possibly misunderstand something so badly? Population genetics is based on the centrality of DNA. It says that evolution takes place because "allele" frequencies change with time (whatever this is supposed to mean). Isn't it obvious, based on the paper we have in front of us, and the discussion that has taken place, that there are cellular processes of regulation which control other cellular processes, which in turn, have phenotypic consequences, all of which has nothing to do with the inheritance of DNA; and, further, are not passed down via DNA. Just look at the most recent post at UD on mouse sperm and siRNAs. The notion that gametes and somatic cells are cut off from one another has fallen apart. IOW, the "infinite allele" model is way wrong. As to NGE, this is an obvious reference to James Shapiro's book. You seem to be completely ignorant of it. What a shame. Finally, that epigenetics has been evoked from a long time ago in order to explain cell differentiation, should not be used as a canard that hopes to deflect away from the tremendous power now being found for various epigenetic effects, and their inheritability for generations.PaV_{January 4, 2016
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Pav, you have said some weird things in your time, but this might take the cake
Furthermore, this widens the crack that has been opened up in traditional pop. gen. by pointing out that ‘changing allele frequencies’ misses quite a lot of what happens in the cell.
Do you really think that anyone claims that cell-biology within an organism has much to do with changing allele frequencies within that organism. I mean, I guess cancer is an evolutionary disease within an organism, but no one claims changes in gene expression during development are about changes in allele frequency. This is so wrong-headed it's hard to know what to do with it. The rest of your post just has the usual claims, without evidence, that everything points to a designer or some mystical force of natural genetic engineering (the last being a particular bizarre claim for an epigenetic effect!)wd400_{January 4, 2016
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wd400:
Certainly the modern enthusiasm for epigenetics has made the word a bit less precise, but it remains the fact the an epigenetic change is a change in gene expression that is not the result of a genetic change. That doesn’t meant the establishment of an epigenetic switch isn’t itself the result of some genetic machinery. Think of the 1st-year biochem example of the lac operon. An epigenetic change encoded in genes.
The problem is that without genetic sequencing we don't know this for sure. Hopefully, with time, this present-day shortcoming will be resolved.
Of course no alleles change in this experiment. But what does change is the degree of histone aceytelation, and that is certainly under genetic control. This experiment establishes that epigentic changes can generate (some of) the caste-specific behaviours of these ants. But it doesn’t say how these epigenetic states are established naturally. We know that these sorts of switches can be the rest of gene-environment interactions (the lac operon, the paper I linked above…) so what’s the big deal.
The "big deal" is that this understanding of how very important phenotypic traits arise points in the direction of NGE---natural genetic engineering. How can you have 'code' without a 'coder'? How can you have an 'engineered' control system without an 'engineer'? All of this points away from the Darwinian point of view, and towards an 'intelligent design' one. Furthermore, this widens the crack that has been opened up in traditional pop. gen. by pointing out that 'changing allele frequencies' misses quite a lot of what happens in the cell.
(BTW, if you’re whole point is that the specification of castes can’t be the result of genetic changes then this paper adds precisely nothing to your argument. It’s been known for a very long time that ants of one caste can be genetically identical to those of another caste, understanding that histone acetylelation plays a part on this doesn’t really change that).
We won't know if "ants of one caste can be genetically identical to those of another caste" until the proper sequencing takes place. I don't know if that has happened as yet, or not. Perhaps you're aware of it. A big part of this post is simply the growing role of 'epigenetics.' It challenges the very foundations of population genetics. We're finding out, more and more, just how much is being inherited from one generation to another via entities other than DNA. You'll have noticed, e.g., the role of siRNAs.PaV_{January 4, 2016
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Certainly the modern enthusiasm for epigenetics has made the word a bit less precise, but it remains the fact the an epigenetic change is a change in gene expression that is not the result of a genetic change. That doesn't meant the establishment of an epigenetic switch isn't itself the result of some genetic machinery. Think of the 1st-year biochem example of the lac operon. An epigenetic change encoded in genes. Of course no alleles change in this experiment. But what does change is the degree of histone aceytelation, and that is certainly under genetic control. This experiment establishes that epigentic changes can generate (some of) the caste-specific behaviours of these ants. But it doesn't say how these epigenetic states are established naturally. We know that these sorts of switches can be the rest of gene-environment interactions (the lac operon, the paper I linked above...) so what's the big deal. (BTW, if you're whole point is that the specification of castes can't be the result of genetic changes then this paper adds precisely nothing to your argument. It's been known for a very long time that ants of one caste can be genetically identical to those of another caste, understanding that histone acetylelation plays a part on this doesn't really change that).wd400_{January 3, 2016
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wd400: You wrote:
It’s both of course. An epigenetic change brought about by a particular allele interacting with an environmental cue. The linked paper is an example of this.
But I had written about ‘changing allele frequencies.’ Alleles are essentially tied to the notion of genes. So, if we talk about an “epigenetic” change, then why is this conflated with a “genetic” change? This only breeds confusion. This is from the paper you linked to:
The evolution of a polyphenism by genetic accommodation relies on two steps: (1) the sensitization of the genetic background, which reveals cryptic genetic variation and makes it accessible to selection, followed by (2) changes in this genetic background so that it becomes enriched in alleles that contribute to environmentally sensitive developmental processes [Roff, 1996; Hazel et al., 2004; Suzuki& Nijhout, 2006).
Sadly, this is undecipherable Darwin-babble, and no more. When I stated that no genetic sequencing had been done, the point being made was that we have no certainty that sequence space is changing; it might simply be, as the study in the OP points out, the result of “deacetylation.” This is from the Science abstract:
Transcriptome and chromatin analyses in the brains of minors treated with HATi and HDACi revealed changes in genes linked to regions of hyperacetylated histone H3 Lys27 (a lysine targeted by CBP) near CBP binding sites. Although untreated majors rarely foraged, suppression of histone deacetylation by injection of HDACi or small interfering RNAs (siRNAs) against the HDAC-encoding gene Rpd3 into young major brains was sufficient to induce and sustain minor-like foraging and scouting for up to 50 days. Strikingly, coinjection of CBP HATi suppressed HDACi-induced foraging and scouting in majors. CONCLUSION Caste-specific foraging and scouting behaviors are tightly linked to morphology and are likely regulated epigenetically by the balance between CBP-mediated acetylation and HDAC-mediated deacetylation of histones in the ant central brain. Thus, behavioral plasticity can be manipulated in the ant C. floridanus by pharmacological and genetic tools that target chromatin regulatory enzymes to stimulate, inhibit, and reprogram behavior.
We’re dealing with living organisms. Nothing here is being transmitted via “common descent.” There is “programming” taking place, and changes within the transcriptome and chromatin using “pharmacological and genetic tools,” with all of this happening in real time. The si-RNAs that are involved, how does that get handled by classical population genetics? There are no "allele" changes taking place, but, rather, changes in RNA expression. All of these kinds of results undermines the centrality of population genetics, defective as it already is. And it points to the way in which the genome is “programmable.” As the OP title reads: Epigenetics, not population genetics, rules.PaV_{January 3, 2016
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It's both of course. An epigenetic change brought about by a particular allele interacting with an environmental cue. The linked paper is an example of this.
BTW, the study you linked to shows that their conclusions is based strictly on phenotypes, and not on any genetic sequencing.
Sure. Classical genetics didn't stop working the day Sanger described DNA sequencing.wd400_{January 2, 2016
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Dionisio: I don't know if the articles are related. I don't think the any of the authors are the same, nor the lab. You'll have to flush that one out for yourself, I'm afraid.PaV_{January 2, 2016
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wd400: OTOH, you say that obviously ant's caste system is governed by 'epigenetics,' and, then, OTOH, you say that phenotypic plasticity is governed by changing allele frequencies. Which is it? BTW, the study you linked to shows that their conclusions is based strictly on phenotypes, and not on any genetic sequencing.PaV_{January 2, 2016
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#4 follow-up Here's something related @1014: https://uncommondescent.com/evolution/a-third-way-of-evolution/#comment-594315Dionisio_{January 1, 2016
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The paper referenced @3 seems kind of old in terms of modern biological research. BTW, the link provided @3 just points at the abstract of the referenced paper. The full paper is referenced @1013 in the following thread: https://uncommondescent.com/evolution/a-third-way-of-evolution/#comment-594304 Note that the given paper fails to answer the important question "where's the beef?". Also, pay attention to the highlighted text @1013 in the above provided link. The referenced paper is talking about adaptations. That's what the Galapagos finch beak shapes story was all about. Built-in adaptation mechanisms embedded within the biological systems.Dionisio_{January 1, 2016
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Since ants of one caste are genetically identical to ants in another it's hardly news that caste-determination is epigenetic. What else could it be? Polyphenisms like this are still the result of changes (or fixations) of allele frequencies -- take a look of this example of a gene controlling a polyphenism http://www.ncbi.nlm.nih.gov/pubmed/18034806wd400_{January 1, 2016
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PaV, is the paper referenced in the below link semi-related to your OP? https://uncommondescent.com/intelligent-design/mystery-at-the-heart-of-life/#comment-594263Dionisio_{January 1, 2016
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PaV Very interesting article. Thank you.Dionisio_{January 1, 2016
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