161 thoughts on “Twins and Epigenetics”

  1. long winded and absurd, These attempts to say genes reflects on our soul are in vain. Its poor sampling. They don’t comp[are the twins with anyone else. everybody does the same things.
    There is no actual evidence to any genetic relationship between different people.
    The start of the article talking about India didn’t help credibility either.

  2. Robert Byers,

    There is no actual evidence to any genetic relationship between different people.

    No, none. That’s why paternity suits always fail.

  3. Allan Miller: Robert Byers, No, none. That’s why paternity suits always fail.

    Because nesting patterns of similarities do not imply common descent. I wonder how many “judeo-christian conservatives” would accept that argument if their offspring were born african-american.

  4. The article does not discuss implications for evolution. Epigenetic modifications can be inherited, but they revert to their original state after about 3 or 4 generations. If a lineage of, say, gibbons gets into a state where all of its members have an epigenetic mark, within a few generations most of them will have reverted to the original state. Only if there have been DNA changes that stabilize the epigenetic modifications will the change remain.

    That is what evolutionary biologists have been trying to point out when creationists and ID advocates loudly declare that epigenetics totally changes thinking about evolutionary biology, and declare that it shows that evolutionary biologists are closed minded. I’m looking at you, Denyse O’Leary.

  5. Here is what I take to be the central point of the article:

    It’s one thing to study epigenetic changes across the life of a single organism, or down a line of cells. The more tantalizing question is whether epigenetic messages can, like genes, cross from parents to their offspring.

    The most suggestive evidence for such transgenerational transmission may come from a macabre human experiment. In September, 1944, amid the most vengeful phase of the Second World War, German troops occupying the Netherlands banned the export of food and coal to its northern parts. Acute famine followed, called the Hongerwinter—the hunger winter. Tens of thousands of men, women, and children died of malnourishment; millions suffered it and survived. Not surprisingly, the children who endured the Hongerwinter experienced chronic health issues. In the nineteen-eighties, however, a curious pattern emerged: when the children born to women who were pregnant during the famine grew up, they had higher rates of morbidity as well—including obesity, diabetes, and mental illness. (Malnourishment in utero can cause the body to sequester higher amounts of fat in order to protect itself from caloric loss.) Methylation alterations were also seen in regions of their DNA associated with growth and development. But the oddest result didn’t emerge for another generation. A decade ago, when the grandchildren of men and women exposed to the famine were studied, they, too, were reported to have had higher rates of illness. (These findings have been challenged, and research into this cohort continues.) “Genes cannot change in an entire population in just two generations,” Allis said. “But some memory of metabolic stress could have become heritable.”

    Both Allis and Reinberg understand the implications of transgenerational epigenetic transmission: it would overturn fundamental principles of biology, including our understanding of evolution. Conceptually, a key element of classical Darwinian evolution is that genes do not retain an organism’s experiences in a permanently heritable manner. Jean-Baptiste Lamarck, in the early nineteenth century, had supposed that when an antelope strained its neck to reach a tree its efforts were somehow passed down and its progeny evolved into giraffes. Darwin discredited that model. Giraffes, he proposed, arose through heritable variation and natural selection—a tall-necked specimen appears in an ancestral tree-grazing animal, and, perhaps during a period of famine, this mutant survives and is naturally selected. But, if epigenetic information can be transmitted through sperm and eggs, an organism would seem to have a direct conduit to the heritable features of its progeny. Such a system would act as a wormhole for evolution—a shortcut through the glum cycles of mutation and natural selection.

    My visit with Allis had ended on a cautionary note. “Much about the transmission of epigenetic information across generations is unknown, and we should be careful before making up theories about the kind of information or memory that is transmitted,” he told me. By bypassing the traditional logic of genetics and evolution, epigenetics can arouse fantasies about warp-speeding heredity: you can make your children taller by straining your neck harder. Such myths abound and proliferate, often dangerously. A child’s autism, the result of genetic mutation, gets attributed to the emotional trauma of his great-grandparents. Mothers are being asked to minimize anxiety during their pregnancy, lest they taint their descendants with anxiety-ridden genes. Lamarck is being rehabilitated into the new Darwin.

    These fantasies should invite skepticism. Environmental information can certainly be etched on the genome. But such epigenetic scratch marks are rarely, if ever, carried forward across generations. A man who loses a leg in an accident bears the imprint of that accident in his cells, wounds, and scars, but he does not bear children with shortened legs. A hundred and forty generations of circumcision have not made the procedure any shorter. Nor has the serially uprooted life of my family burdened me, or my children, with any wrenching sense of estrangement.

  6. Hi walto

    The article’s mention of entomological epigenetics caught my eye!

    As Joe and others have mentioned here

    …the term Neo-Darwinism requires meticulous and careful parsing.

    Meiosis’ clear differences from mitosis prompted Weisman to propose his famous Germ Plasm theory which proposed a correction to Darwin’s fatal error of “Pangenesis” and the inheritance of acquired characteristics. The famous “Weisman Barrier” & his “Germ Plasm Theory” distinguished somatic cells from reproductive cells. Weismann was the first to understand cell fate during development in terms of a totipotent germ line vs. differentiated somatic cells. His reasoning was intellectually elegant, premised as it was on a variety of biological phenomena such as sterile worker and soldier drones in insect colonies (not to mention “Chromatin Diminution”) which taken all together necessarily contradicted the possibility of Darwin’s Pangenesis and the acquisition of acquired traits by use and disuse as postulated by Darwin (Lamarck’s version was subtly different) and later dismissed by Darwin’s contemporaries.

    Julian Huxley had in the meantime, already conceded the “eclipse of Darwinism”; in no small part due to persistent confusion about inheritance. Weismann realized that any rejection of biblical Creationism must necessarily oblige an embrace of Evolution to explain Biological diversity. On that premise (and embracing Darwin’s total and absolute rejection of the metaphysical) Weismann became obsessed with heredity and its role in Evolution. August Weismann was an intellectual giant who built on the observations of his predecessors and Weismann was the first to integrate all these scientific advances and insights into a rescue of Darwin’s great idea which he named “Neo-Darwinism”.

    The fact Weismann is given such short shrift in modern textbooks is most unjust IMHO.

    Maybe my own German DNA is kicking in, but we may just need to resurrect Neo-Weismanism.

    (… actually that was to be the subject of my next OP)

  7. Hi, Tom.

    I’m still wondering about your take on Butler’s claim (reproduced as a comment to your recent thread on this subject) that Lamarck was a proponent of natural selection. Is my suspicion that you are a closet Butlerian correct?

  8. Joe Felsenstein:
    The article does not discuss implications for evolution.Epigenetic modifications can be inherited, but they revert to their original state after about 3 or 4 generations.

    Hi Joe

    The article does not discuss implications for evolution. Epigenetic modifications can be inherited, but they revert to their original state after about 3 or 4 generations.

    That last statement is not at all clear to me as it would appear that a precise definition of the term epigenetics seems to be akin to nailing Jello to the wall.
    Clearly such tags can on rare occasion continue across generations:

    In Linaria vulgaris
    In Drosophila
    In rats
    In mice

    On an earlier thread I reposed the question to Allan Miller

    Part of the confusion here would be a definition of our terms: what exactly is “epigenetics” and what “epigenetics” is not.

    … it might be helpful in our exchange if we identified all the instances of when exactly epigenetic erasure/rewriting actually occurs; I mean besides gender specific resets during gamete formation by PGC and what appear to be maternal-specific resets immediately following fertilization.

    The problem is that SOME of what is called so-called epigenetic states can be inherited through a round of meiosis and fertilization along the lines of erasure and gender specific rewriting.

    Whereas OTHER so-called epigenetic states can escape this meiosis and fertilization erasure/rewrite process… (Igf2 jumps to mind)

    It could be argued that gender specific resets in and of themselves, serve some adaptive function n’est-ce pas?

    Meanwhile, you and I discussed this on an earlier occasion where again I admit I am in over my head and I am preemptively grateful if you were to indulge me here.

    In my exchange with Allan, I imagined (3-4) multigenerational epigenetic inheritance as some ‘toggle-switch’ which is supposed to be adaptive because children typically experience the same conditions as their parents but at the same time allows quick resets along Ptashne’s version of Lambda autogenous regulation of lysogeny because ancestral responses would be detrimental if the environments of the progeny and the ancestors were different.

    Parenthetically, I also think the Igf2 similarities to Lambda maintenance of Lysogeny are telling – In fact, many parallels with the Trp Operon also exist. Expression of the Tryptophan Repressor protein is also regulated by its own protein product by a process called “autogenous regulation”. The Trp repressor binds to an operator that precedes the Trp gene itself thereby keeping repressor levels low (about 20-30 molecules per cell!!!) allowing the system to be VERY responsive to Tryptophan fluctuations and in the case of Lanbda, very sensitive to environmental signals.

    I think what we are witnessing the eukaryotic equivalent of “autogenous regulation” as extremely fine-tuned by the positive feedback commitment steps described by Ptashne… that’s what my gut tells me.

    That means the very possession of what is called epigenetics (as described in this article) is in of itself an adaptation – the previous exaptation having been retroelement silencing

  10. walto:
    Hi, Tom.

    I’m still wondering about your take on Butler’s claim (reproduced as a comment to your recent thread on this subject) that Lamarck was a proponent of natural selection.Is my suspicion that you are a closet Butlerian correct?

    I need to get back to you…

    Family beckons

    Let’s say quickly that I agree with Gould and I disagree with John Harshman given my reading of Lamarck in the original French.

    I understand that Gould was frequently prone to hubris (in excelsis)

    This time Gould may actually have understated his thesis.

    I never heard of Butler until you and Joe mentioned him… again, I will need to get back to you on that.

    best

  11. TomMueller,

    You are mistaking walto’s question. It has nothing to do with our disagreement, which was about Lamarck and common descent. This is about Lamarck and natural selection. Is it your claim that Lamarck was a proponent of natural selection? If so, that’s something new.

  12. John Harshman:
    TomMueller,

    You are mistaking walto’s question. It has nothing to do with our disagreement, which was about Lamarck and common descent. This is about Lamarck and natural selection. Is it your claim that Lamarck was a proponent of natural selection? If so, that’s something new.

    Hi John

    I should have said “tentatively” disagree with you

    Some of what I have read in Lamarck (especially some of his Botany) seems to be suggestive of “Natural Selection” when Lamarck discusses the emergence of new species in response to “les circonstances”

    His definition of speciation according to reproductive isolation is remarkably prescient IMHO

    Key words – “TENTATIVELY” and “SEEMS”

    I need to see what Butler wrote to prevent any reinvention of the wheel…

    Meanwhile – I am busy with other projects and will need to get back to walto (and you) on that.

  13. First off, thank you walto! I note how many times the word “memory” appears in the article. I’ve gotten tons of flak at TSZ for saying epigenome = RAM. The erasable, rebootable, reversible, read-writable quality of the God-made epigenome makes it analogous to Random Access Memory (RAM) in the man-made world of computers.

    Epigenetic Memory Changes during Embryogenesis

    DNA is not just a static read-only memory (ROM) for coding proteins, but hosts dynamic random access memory (RAM) in the form of methylations and histone modifications for regulation of gene expression, cellular differentiation, learning and cognition, and who knows what else. ….at least some of the roles of non-coding DNA are involved in supporting the complex epignomic memory in each cell.

    compares well with the article, for example:

    Had Allis started his experiments in the nineteen-eighties trying to pin down words like “identity” and “memory,” he might have found himself lost in a maze of metaphysics. But part of his scientific genius lies in radical simplification: he has a knack for boiling problems down to their tar. What allows a cell to maintain its specialized identity? A neuron in the brain is a neuron (and not a lymphocyte) because a specific set of genes is turned “on” and another set of genes is turned “off.” The genome is not a passive blueprint: the selective activation or repression of genes allows an individual cell to acquire its identity and to perform its function. When one twin breaks an ankle and acquires a gash in the skin, wound-healing and bone-repairing genes are turned on, thereby recording a scar in one body but not the other.
    …
    Now there are meetings on the epigenetics of human memory, of ants, of cancer, of mental illness. Part of the reason for the excitement is that epigenes may be vastly more tractable than genes. “Gene therapy was all the rage when I began my career, but manipulating genes has turned out to be much harder than envisioned,” Allis said. Genes, after all, are the permanent repository of a cell’s information system, and thus more tamperproof. (If genes are hardware, epigenes are firmware.)

    Joe said this:

    Joe Felsenstein:

    That is what evolutionary biologists have been trying to point out when creationists and ID advocates loudly declare that epigenetics totally changes thinking about evolutionary biology, and declare that it shows that evolutionary biologists are closed minded. I’m looking at you, Denyse O’Leary.

    Most ID advocates don’t understand this stuff. But it does relate indirectly to Dan Graur’s assertion about the hudreds of millions the NIH is spending on ENCODE (and sister projectes Roadmap and E4):

    If ENCODE is right, evolution is wrong.

    Dan Graur

    The question epigenetics in terms of histone modifications and DNA methylations does raise issues related to mutational load indirectly because a lot of the genome that has been thought to be junk has been found to participate in critical cellular function because the epigenome is critical to ability to live. ENCODE has contributed to the discovery of function in the DNA as a scaffold for the epigenome. By the way, the article used the word scaffold. Note recently I said the same related to the epigenome:

    The picture in the OP above demonstrates utility of the non-coding regions as scaffolds for the epigenomes of each cell. We’d be dead without such “junk” DNA to host the epigenetic memories or places for molecular machines to park.

    At some point if a certain proportion of the genome is under functional constraint, it would be as Dan Graur says, “evolution is wrong.” ENCODE has certainly raised the prospect that more of the genome is under constraint than thought, but we’re only beginning to explore the question. ENCODE researchers have their opinions. 🙂

    Some of the epigenomic function is related to what was thought to be junk (one example is the HOTAIR lincRNA, and probably many more to be found). The techniques Allis developed fueled a lot of the ENCODE research which Dan Graur hates. ENCODE not only studies the genome but the epigenome. ENCODE and sister projects at the NIH now have a projected total budget of 793 million, maybe half of that already spent. The diagram below show many of the genetic and epigenetic experiments by ENCODE. One experiment was specifically pioneered by Allis (CHiA-PET). Some of the epigenomic studies by ENCODE are the WGBS (Whole Genome Bisulfite Sequencing) and RRBS (Reduced Representation Bisulfite Sequencing). Some texts allow RNA to be defined as part of the epigenome. Clip-Seq and Rip-seq are used by the ENCODE consortium to explore these RNA epigenetic factors as well.

    Even though the DNA codes for protein sequences, we really don’t know where a lot of developmental information resides — it could well reside in the cytoplasm and glycol protein complexes or who knows where. It is heritable.

    Example: we put human insulin genes into bacteria through genetic engineering. The hybrid cell really doesn’t become human like. We could imagine shoving tons more human DNA into a bacterial cell, and unless the cell’s general organization gets totally rewired, the heritable form will always be bacteria like. Much of the heritable template may not be solely the protein sequence, hence DNA is only half the story, especially in Eukaryotes.

    The NIH Glycan group argues more than half of the information processing in the cell is due to glycans. Proteins are also information bearing. We don’t know the extent of heritable glyco/protein information but a few researchers assert the protein interactome (not merely the protein sequences defined by DNA) are heritable and serve as a template to the next generation of individuals.

    This form of heritable information may not be as mutable as DNA, hence it would be a barrier to macro evolution.

    If one wants to be a philosophical naturalist, that’s up to them, but as I alluded to in Does Naturalism Exclude Exceptional Phenomenon, I think what makes life special is a process we probably do not have direct experimental access to. Allis work as mentioned in the article reinforces my that life is the product of exceptional processes.

  14. stcordova: I’ve gotten tons of flak at TSZ for saying epigenome = RAM. The erasable, rebootable, reversible, read-writable quality of the God-made epigenome makes it analogous to Random Access Memory (RAM) in the man-made world of computers.

    Or maybe it is more analogous to EEPROM (electrically erasable programmable read only memory).

  15. Btw, Tom, even if you don’t know Butler’s writings on evolution, you should have heard of him. He wrote The Way of All Flesh and (the awesome) Erewhon, as well as one of the greatest (and funniest) critiques of Biblical literalism ever written, The Fair Haven. He had some of the weirdest views of everything that anybody ever had. (I’ve mentioned a couple of his crazy views in an earlier post, but there are so many others that it’s sometimes hard to believe he was serious–but…he was.)

    Besides all that, he was a painter and wrote an opera (in the style of Handel). And, with Swift, Wilde and Mencken, was among the most quotable English adage writers who ever lived. Really fun to read.

  16. walto,

    I’ve gotten tons of flak at TSZ for saying epigenome = RAM. The erasable, rebootable, reversible, read-writable quality of the God-made epigenome makes it analogous to Random Access Memory (RAM) in the man-made world of computers.

    Except it doesn’t. If a particular base is methylated, it’s just another switch, so it turns a 4 position switch (ACTG) into a 5 (ACTGmC). You couldn’t store a picture of your mom in an ‘epigenome’ without seriously screwing with the genome. You get flak for it because it’s a dumb idea.

  17. Joe Felsenstein:
    The article does not discuss implications for evolution.Epigenetic modifications can be inherited, but they revert to their original state after about 3 or 4 generations.If a lineage of, say, gibbons gets into a state where all of its members have an epigenetic mark, within a few generations most of them will have reverted to the original state.Only if there have been DNA changes that stabilize the epigenetic modifications will the change remain.

    That is what evolutionary biologists have been trying to point out when creationists and ID advocates loudly declare that epigenetics totally changes thinking about evolutionary biology, and declare that it shows that evolutionary biologists are closed minded.I’m looking at you, Denyse O’Leary.

    Changing a word doesn’t change its essence.
    If some trait is being passed on with selection pressures then its a defeat for the core of evolution. Evolutionism was to EXPLAIN traits being passed on and so explain the changes. Otherwise all minor changes, needed to evole stuff, would never stick. They would never change the dna. Too little difference.
    If Epi is admitted and then its said later generations revert back then it shows several points.
    The bodies do easily innately adapt. And unless thresholds are passed they won’t stick.
    Thus all biological change can be seen as merely an issue with threshold. epi proves how easily things change and pass on. The only problem is threshold not being crossed.
    Therefore epi shows a option for innate triggers to change our bodies.
    Passing on a trait is no small deal. Something is sticking.
    Just tweek the stickyness spectrum and you have your change.
    No selection on mutations need apply which is very unlikely anyways.

  18. ,

    You couldn’t store a picture of your mom in an ‘epigenome’ without seriously screwing with the genome.

    That’s because the memory in the epigenome stores information critical for living, a putting photos would mess up the critical data stored there. You’re just straining at words. The article uses the word memory about 18 times to describe the function of the epigenome.

    Besides the epigenome is part of the mechanism implementing human memory which actually does remember images!

  19. From the Stem Cell Handbook 2013, the chapter entitled “Quantitative Approaches to Model Pluripotency and Differentiation in Stem Cells”

    http://link.springer.com/chapter/10.1007/978-1-4614-7696-2_4?no-access=true

    Epigenetic memory may be defined as a set of gene product concentrations and gene activity by levels in the cell. This information is analogous to random access memory of computers (RAM)… The discrete genome has analogy to read-only memory of computer devices (ROM)

    You were saying, Allan, about my “dumb” idea of the eigenome’s analogy to RAM?. Actually it looks like I was like minded with some pretty smart researchers. Get a load of the diagram! Hahaha!

  20. stcordova,

    That’s because the memory in the epigenome stores information critical for living, a putting photos would mess up the critical data stored there. You’re just straining at words. The article uses the word memory about 18 times to describe the function of the epigenome.

    I’m straining at words! If you’re insisting it’s ‘like RAM’, it’s not. So now you cling to the fact that they say ‘memory’ a few times. My chair has a memory of my ass. That’s not like RAM either.

    Besides the epigenome is part of the mechanism implementing human memory […]

    Prove i

  21. Once again I find myself put in my place by ‘others’. “Look at all these people who think translation involves a ‘true code'”. “Look at all these people who use the RAM analogy”. “Look at all these people who think epigenetics Blows Darwin Out The Water”. I’ll start giving a damn about their opinion when you start giving an equivalent damn about the many people who think YEC/ID is a crock. ‘Til then, what care I for the opinions of ‘others’?

  22. What do you think of that diagram in the ,Stem Cell Handbook. How do you like them apples? ::-)

    Besides the epigenome is part of the mechanism implementing human memory

    Well gee Allan, read it and weep:

    http://www.jneurosci.org/content/30/10/3589

    It has been established that regulation of chromatin structure through post-translational modification of histone proteins, primarily histone H3 phosphorylation and acetylation, is an important early step in the induction of synaptic plasticity and formation of long-term memory. In this study, we investigated the contribution of another histone modification, histone methylation, to memory formation in the adult hippocampus. We found that trimethylation of histone H3 at lysine 4 (H3K4), an active mark for transcription, is upregulated in hippocampus 1 h following contextual fear conditioning. In addition, we found that dimethylation of histone H3 at lysine 9 (H3K9), a molecular mark associated with transcriptional silencing, is increased 1 h after fear conditioning and decreased 24 h after context exposure alone and contextual fear conditioning. Trimethylated H3K4 levels returned to baseline levels at 24 h. We also found that mice deficient in the H3K4-specific histone methyltransferase, Mll, displayed deficits in contextual fear conditioning relative to wild-type animals. This suggests that histone methylation is required for proper long-term consolidation of contextual fear memories. Interestingly, inhibition of histone deacetylases (HDACs) with sodium butyrate (NaB) resulted in increased H3K4 trimethylation and decreased H3K9 dimethylation in hippocampus following contextual fear conditioning. Correspondingly, we found that fear learning triggered increases in H3K4 trimethylation at specific gene promoter regions (Zif268 and bdnf) with altered DNA methylation and MeCP2 DNA binding. Zif268 DNA methylation levels returned to baseline at 24 h. Together, these data demonstrate that histone methylation is actively regulated in the hippocampus and facilitates long-term memory formation.

  23. stcordova,

    Well gee Allan, read it and weep:

    Boohoo. Nonetheless, you are confusing 2 completely different aspects of the general term ‘memory’.

  24. I said:

    the epigenome is part of the mechanism implementing human memory

    Allan disputed this, and demanded proof. I provided 1 reference, here is another:

    http://link.springer.com/chapter/10.1007/978-3-642-27913-3_7?no-access=true

    The Role of Histone Acetylation in Long-Term Memory Storage
    …

    Note, I didn’t say human memories are stored in histones, but rather the epigenome (of which histones are a part) are involved in the process of remembering. The epigenetic memory stored in the histones in each nerve cell appear important in these memory cells remembering their epigenetic state and memory state hence then do help form part of our memory mechanism. Epigenetic memory is linked to brain memory.

  26. Am I wrong to think that epigenetics, in the popular press, has taken on the aura of Lysenkoism?

    It seems to me that there is a desperate need on the part of some people to believe that acquired traits can be inherited.

  27. Epigenetics no longer in the literature even necessarily implies inheritance — histone epigenetic marks can change in cells without being inherited. The term is becoming a misnomer, but a rose is a rose by any other name.

  28. stcordova: Epigenetics no longer in the literature even necessarily implies inheritance

    Ultimately, how does any of this support Jesus?

  30. Epigenetics has become a kind of Lysenkoism among IDists, and apparently, among some people who would like some sort of social change.

    Strange bedfellows.

  31. Thanks for that Bruce. I just tweeted that Vox piece (although Vox has many, many, many more followers than I do). I’m fairly ignorant about this stuff, and I don’t like being taken advantage of by the NYer. I assumed that article had been vetted by competent scientists. Guess I shouldn’t have.

  32. petrushka:
    Epigenetics has become a kind of Lysenkoism among IDists, and apparently, among some people who would like some sort of social change.

    Strange bedfellows.

    Evolution just has to be wrong, it has to be. And Darwin didn’t mention epigenetics, so, you know…

    Evolution is just wrong and something proves it!

    Glen Davidson

  33. I didn’t get the sense that the author of the article thinks evolution is wrong. If the Vox piece is right, he simply makes mistakes about prevailing views of epigenitic mechanisms. It’s not an anti-evolution story, just a confused one.

  34. walto:
    I didn’t get the sense that the author of the article thinks evolution is wrong.If the Vox piece is right, he simply makes mistakes about prevailing views of epigenitic mechanisms.It’s not an anti-evolution story, just a confused one.

    I didn’t think that petrushka was aiming at the New Yorker writer, although it’s possible for all that I know. For myself, I certainly wasn’t.

    Glen Davidson

  36. This undark article makes the same main point as what I take the Vox article to be making: namely, that the author and his editors placed the goal of telling a good story ahead of the goal of presenting the science accurately and completely.

    The undark article also links to two posts from Coyne, the second of which contains two letters to the editor addressing the problems with the original article in detail. According to Coyne, the New Yorker has refused to publish those letters.

  37. For some reason … I am reminded of a favourite exchange in a favourite movie:

    Otto West: Don’t call me stupid.

    Wanda: Oh, right! To call you stupid would be an insult to stupid people! I’ve known sheep that could outwit you. I’ve worn dresses with higher IQs. But you think you’re an intellectual, don’t you, ape?

    Otto West: Apes don’t read philosophy.

    Wanda: Yes they do, Otto. They just don’t understand it. Now let me correct you on a couple of things, OK? Aristotle was not Belgian. The central message of Buddhism is not “Every man for himself.” And the London Underground is not a political movement. Those are all mistakes, Otto. I looked them up.

  38. This is the part that Sal obtusely still cannot wrap his head around:

    Is there sometimes (not always) an aspect of inter-generational memory (metaphorically speaking) to epigenetics?

    Without belaboring the finer details – short answer = yes.

    Next question:

    Would nucleosome modification (including Histone acetylation) play some role in the expression of this so-called “memory” effect?

    Again, the short answer is “yes”.

    But herein lies the rub – nucleosome modification is a result and NOT a cause of epigenetics

    … a point that Sal has repeatedly been attempting to deny in a confused and often incoherent series of contradictory posts

    BUT (drum roll please) happens to be the very point made in the citation that Sal has just tossed our way!

    …for further elucidation of Sal’s lack of lucidity please refer to

    Epigenetic Memory Changes during Embryogenesis

    BASTA!

  39. walto: I didn’t get the sense that the author of the article thinks evolution is wrong.

    That’s not what I wanted to imply.

    My thought is that there’s an indecent similarity between the way creationists are describing epigenetics and the way some non-specialist science writers are describing it. It parallels the confusion about junk DNA.

  41. http://www.vox.com/2016/5/7/11606886/scientists-angry-new-yorker-epigenetics

    The New Yorker piece agrees with the way epigenetics is taught at the NIH and by supporters of the NIH ENCODE consortium.

    One of the scientists cited as angry was Jerry Coyne who is an evolutionary biologist who hardly holds a candle to molecular biologists like Allis or the Nobel Laureates who contributed to the field of histone research and epigenetics. Allis is cited my chromatin classes, Coyne isn’t.

  43. This undark article makes the same main point as what I take the Vox article to be making: namely, that the author and his editors placed the goal of telling a good story ahead of the goal of presenting the science accurately and completely.

    The undark article also links to two posts from Coyne, the second of which contains two letters to the editor addressing the problems with the original article in detail. According to Coyne, the New Yorker has refused to publish those letters.

    I disagree. My NIH claases agrees with New Yorker article. My class counts as credit for doctoral students in cellular biology at my Alma Mater, Johns Hopkins. Coyne needs to but out, this isn’t his area of expertise. This isn’t the first time he’s butted heads with molecular biologists.

  44. stcordova: The New Yorker piece agrees with the way epigenetics is taught at the NIH and by supporters of the NIH ENCODE consortium.

    When Sal is WRONG – he is not simply WRONG, but is in fact SPECTACULARLY WRONG!

    Wally Gilbert and Sidney Altman are Noble Prize laureates in the field of Molecular Genetics and definitely know what they are talking about.

    Contrary to Sal’s suggestion, Tom Maniatis, Richard Mann, John Greally, Oliver Hobert, & Steve Henikoff are

    1 – also famous in the field of Molecular Genetics and …

    2 – all funded by NIH as can can be confirmed here:

    http://www.brimr.org/NIH_Awards/2012/AllOrgDeptPI_2012.xls

    What do all of these esteemed scientists have in common?

    They are ALL unanimous that Mukherjee got not only got the Epigenetics story wrong, but that Mukherjee got the Epigenetics story horribly WRONG!

    http://tinyurl.com/h36k537

    What was Mukherjee’s cardinal sin of ommission according to such esteemed expert opinion?

    Regulatory proteins called “transcription factors”, and not the “epigenetic markers” of nucleosome modification (including Histone acetylation) are central to understanding epigenetics.

    Yet again – Sal fails to understand that nucleosome modification is a result of and not a cause of epigenetics.

    I am begging to feel like Bill Murray’s character in the movie Goundhog Day

  45. OMagain:

    stcordova: Epigenetics no longer in the literature even necessarily implies inheritance

    Ultimately, how does any of this support Jesus?

    I’m glad to see someone is keeping his eye on the ball.

  46. From the New Yorker article:

    Ants have a powerful caste system. A colony typically contains ants that carry out radically different roles and have markedly different body structures and behaviors. These roles, Reinberg learned, are often determined not by genes but by signals from the physical and social environment. “Sibling ants, in their larval stage, become segregated into the different types based on environmental signals,” he said. “Their genomes are nearly identical, but the way the genes are used—turned on or off, and kept on or off—must determine what an ant ‘becomes.’ It seemed like a perfect system to study epigenetics. And so Shelley and I caught a flight to Arizona to see Jürgen Liebig, the ant biologist, in his lab.”

    So, why do the ants have different development. Is it because they have different genomes or different epigenomes?

  47. stcordova: Is it because they have different genomes or different epigenomes?

    It’s because Jesus wants it that way.

  48. I think it’s useful to think of ants as cells. They all have the same genome, but they develop different due to chemical signals encountered early in development.

    This is how individual ants can appear altruistic. Anything a individual ant, or individual cell does to contribute to the survival of the body/colony contributes to the survival of the common genome.

  50. stcordova,

    One of the scientists cited as angry was Jerry Coyne who is an evolutionary biologist who hardly holds a candle to molecular biologists like Allis or the Nobel Laureates who contributed to the field of histone research and epigenetics. Allis is cited my chromatin classes, Coyne isn’t.

    You know there are Nobel laureates who think Creationism is a pile of garbage, don’t you? It’s funny the way you (and many of your ilk) portray people who appear to agree with you as giants in their field, the rest mere intellectual maggots.

    “Nobel Laureate X says”. One can get pretty good odds that the author of such a sentence is a Creationist.

    Ask Allis if he thinks epigenetics evolved.

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