161 thoughts on “Twins and Epigenetics

  1. stcordova,

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

    What does this have to do with the price of fish? Differential regulation is indeed a thing. That’s why you’re not a blob of cells.

  2. Regarding Shelley Berger’s work on ants reported in the New Yorker:

    http://genome.cshlp.org/content/23/3/486.long

    Abstract

    In many ant species, sibling larvae follow alternative ontogenetic trajectories that generate striking variation in morphology and behavior among adults. These organism-level outcomes are often determined by environmental rather than genetic factors. Therefore, epigenetic mechanisms may mediate the expression of adult polyphenisms. We produced the first genome-wide maps of chromatin structure in a eusocial insect and found that gene-proximal changes in histone modifications, notably H3K27 acetylation, discriminate two female worker and male castes in Camponotus floridanus ants and partially explain differential gene expression between castes. Genes showing coordinated changes in H3K27ac and RNA implicate muscle development, neuronal regulation, and sensory responses in modulating caste identity. Binding sites of the acetyltransferase CBP harbor the greatest caste variation in H3K27ac, are enriched with motifs for conserved transcription factors, and show evolutionary expansion near developmental and neuronal genes. These results suggest that environmental effects on caste identity may be mediated by differential recruitment of CBP to chromatin. We propose that epigenetic mechanisms that modify chromatin structure may help orchestrate the generation and maintenance of polyphenic caste morphology and social behavior in ants.

  3. stcordova: Regarding Shelley Berger’s work on ants reported in the New Yorker:

    In what way does that support Creationism?

  4. Sal:

    Blah, blah, blah, hundreds of completely irrelevant words….

    Therefore YEC and Jesus.

    It is cold comfort that there are New Yorker quality writers out there doing the same shit.

    Here’s a clue, Sal: Vernalization died with Lysenko. It is amusing in a sick sort of way that IDists are trying to reanimate Stalin’s geneticist.

  5. 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

    I don’t have a problem with these guys disagreeing with the article, because they are qualified, which is more than I can say for Coyne.

    As far as those who would be favorable to the New Yorker article, this lays out the battle lines:

    I have observed this phenomenon over more than 30 years now: in the 80s, studies of transcriptional regulation fell into two clear camps, one the biochemists/geneticists, carrying on the work started by Jacob and Monod to show how transcription factors activate and repress genes, and how the basic mechanisms are conserved between prokaryotes and eukaryotes; the other, influenced strongly by structural biologist/chemists such as Gary Felsenfeld (a student of Linus Pauling), investigating “chromatin structure”, identifying features that correlate with gene expression such as hypersensitive sites (I guess this group was inspired by structural biology’s one unambiguous huge success: the DNA double helix and the subsequent molecular biology zeitgeist of biological insights from structure.)

    https://whyevolutionistrue.wordpress.com/2016/05/05/the-new-yorker-screws-up-big-time-with-science-researchers-criticize-the-mukherjee-piece-on-epigenetics/

    My professors work in Felsenfeld’s NIH lab, so you know which side I’m going to be on.

    As to this comment about Allis and Reinberg being controversial:

    Not only does he represent the ideas propagated by Dr. Allis and Dr. Reinberg as set in stone, which they are not; in fact, many researchers actively debate whether the ‘epigenetic’ processes they study have indeed a causative, instructive role in gene regulation or whether they are just cogs downstream of proteins, known as ‘transcription factors’,

    Note the authors on this textbook on epigenetics! Does a certain crowd of guys not like the direction of textbook biology being driven by Allis and Reinberg and the ENCODE consortium?

  6. One of the anti-New Yorker Nobelists:

    Sidney Altman, Sterling Professor of Molecular, Cellular, and Developmental Biology and Chemistry at Yale University, Nobel Laureate:

    I am not aware that there is such a thing as an epigenetic code. It is unfortunate to inflict this article, without proper scientific review, on the audience of The New Yorker.

    Well if he looked at Wikipedia, he might give a more charitable rendering:

    https://en.wikipedia.org/wiki/Epigenetic_code

    The epigenetic code is hypothesised to be a defining code in every eukaryotic cell consisting of the specific epigenetic modification in each cell. It consists of histone modifications defined by the histone code and additional epigenetic modifications such as DNA methylation. The base for the epigenetic code is a system above the genetic code of a single cell. While in one individual the genetic code in each cell is the same, the epigenetic code is tissue and cell specific.[1] The epigenetic code can be multidimensional in nature. It could include any of the three major cellular macromolecucles; namely, DNA (code independent), RNA, and/or protein. In some ciliates potential structural codes have also been suggested.[2]

  7. Sal, evo/devo is not exactly new.

    The wormhole to evolution is simply bullshit.

  8. Walto,

    My opinion and speculation only. I think there is an issue of reputation, prestige and grant money in play. Allis and friends have the ear of those holding the dollars especially for medical research. The Epigenetic Therapeutic market is estimated to be growing. The NIH has already cast big money in epigenetics.

    One side (as represented in Coyne’s post) is not looking like they will be on the receiving end of future prestige and money:

  9. stcordova:… this lays out the battle lines:

    There are no more “battle lines”! You lost the battle long ago! You forgot to attend your own funeral!

    stcordova: My professors work in Felsenfeld’s NIH lab, so you know which side I’m going to be on.

    Great! Then do what you promised long ago and invite your professors to adjudicate. Ask them if you are on the correct side of any imaginary battle lines?

    Until that happens – your failure constitutes a public and tacit admission of defeat!

  10. The is money and prestige in epigenetics:

    http://www.nature.com/nrd/journal/v5/n1/full/nrd1930.html

    Epigenetic therapy of cancer: past, present and future

    Christine B. Yoo & Peter A. Jones

    Abstract

    The initiation and progression of cancer is controlled by both genetic and epigenetic events. Unlike genetic alterations, which are almost impossible to reverse, epigenetic aberrations are potentially reversible, allowing the malignant cell population to revert to a more normal state. With the advent of numerous drugs that target specific enzymes involved in the epigenetic regulation of gene expression, the utilization of epigenetic targets is emerging as an effective and valuable approach to chemotherapy as well as chemoprevention of cancer.

    This shows Allis’ views are commanding respect:

    http://epigenie.com/epigenetic-drugs-more-than-hype-in-the-pipeline/

    The first generation of FDA-approved epigenetics-based drugs has firmly established that epigenetic modulation is a viable treatment option for a growing list of diseases. The four epigenetic drugs available for clinical use in the U.S. include two DNA demethylating agents, 5-azacytidine and decitabine, and two histone deacetylase (HDAC) inhibitors, vorinostat and valproic acid. The latter two drugs work by blocking HDACs, enzymes that remove acetyl groups from histone tails. 5-azacytidine and decitabine inhibit DNA methyltransferase enzymes, causing reduced overall levels of DNA methylation. Both classes of epigenetic drugs are thought to function, at least in part, by de-repressing genes silenced in disease, such as tumor suppressor genes.

  11. stcordova:
    … random cut&paste incoherent bovine doodoo

    Of course you are incorrect… yet again, and you demonstrate as much by failing to invite your own professors to adjudicate as promised.

  12. Sal, quit shitting your pants and tell us what this has to do with evolution. Particularly, how does the environment affect future generations?

  13. Then do what you promised long ago and invite your professors to adjudicate.

    I never made such a promise. If I said something that made you think that, that was not what I intended to say. Show TSZ where a promise was explicitly made, provide a quote, or otherwise retract your false claim.

  14. stcordova: I never made such a promise. If I said something that made you think that, that was not what I intended to say. Show TSZ where a promise was explicitly made, provide a quote, or otherwise retract your false claim.

    stcordova: I never made such a promise. If I said something that made you think that, that was not what I intended to say. Show TSZ where a promise was explicitly made, provide a quote, or otherwise retract your false claim.

    I have no idea whether you made an explicit promise, but you have implied that your professors agree with you.

    So put up or shut up.

  15. Sal, quit shitting your pants and tell us what this has to do with evolution. Particularly, how does the environment affect future generations?

    The OP had nothing much to do with evolution did it? The OP does suggest how immensely complex biological systems are (an epigenetic code for each cell type — WOW!), which sort of flies in the face of the junk-proponents like Graur and Moran.

    Many environmentally induced epigenetic marks are not inherited, but reset. A few persist, but the issue of epigenetics is the layers of complexity that it adds to biology. ENCODE has helped uncover this layer and explicitly used at least one of Allis’ experimental techniques (ChIA-PET), and it doesn’t sit well with Graur:

    If ENCODE is right, evolution is wrong.
    — Dan Graur

    and

    the evolution-free philosophy of ENCODE has not started in 2012. The only difference is that Friedrich Vogel was an honest scientist in a world in which disciplines were rigidly compartmentalized. In comparison, no such excuses exist for ENCODE. My only explanation for their continuing existence is that the wannabe ignoramuses, self-promoting bureaucrats, and ol’ fashion crooks of ENCODE are protected from criticism and penalties for cheating by the person who gives them the money. Thus, they can continue to take as much money from the public as their pockets would hold, and in return they will continue to produce large piles of excrement that are hungrily consumed by gullible journalists who double as Science editors.

    Dan Graur

    ENCODE (with Roadmap and E4) ~ $793 million. More likely to follow.

    Looks like the prestige and money are going to ENCODE not so much to Dan Graur. Imho, just an opinion, Graur sounds kindda whiney that he isn’t getting a piece of the prestige and money pie.

  16. Sal,
    If evolution is wrong does that mean creationism is therefore true?

    How does it support you in any way if evolution X is replaced with evolution Y, where neither X nor Y offer any support to any telic intervention nor creationism?

    You might as well just pick a contentious topic in biology where many experts disagree and use the mere fact of that disagreement as some sort of evidence for your own veiled agenda.

    Oh, wait now…

  17. stcordova: The OP had nothing much to do with evolution did it? The OP does suggest how immensely complex biological systems are (an epigenetic code for each cell type — WOW!), which sort of flies in the face of the junk-proponents like Graur and Moran.

    No, it doesn’t.

  18. petrushka: but you have implied that your professors agree with you.

    Everything is implied with Sal.

    Here’s another quote from Dan for you Sal:

    Dan Graur

    Because genomes are products of natural processes rather than intelligent design, all genomes contain functional and nonfunctional parts.

    The problem is when you glue your worldview from lots of little pieces of other peoples that you think support you then you are unable to produce anything new as you don’t have a coherent workspace.

    So, If ENCODE is right and evolution is wrong then intelligent design continues to be wrong. And that’s according to Dan Graur. But don’t let that stop you slyly misrepresenting him and using slices of his world to compose your own. It’ll fall apart in the end.

  19. petrushka: No, it doesn’t.

    Ah, he did say “sort of” which is more than enough wriggle room.

    C’mon Sal, explain yourself.

    Systems that have junk can’t be complex – discuss!

  20. Here is a free PDF of the opening pages of Allis’ textbook. Chapter’s were reading materials for my chromatin class.

    http://cshlpress.com/pdf/sample/2014/epigenetics2/EPIFM.pdf

    The preface shows some of the things I’ve posted about at TSZ in the face of the usual litany of “Sal is clueless, confused,” blah blah blah.

    Despite this, there were the naysayers and critics of Allis mentioned on Coyne’s blog — reminds me of Graur calling the ENCODE scientists crooks and ignoramuses.

    You can inherit something beyond the DNA sequence. That’s where the real excitementis now” (Watson 2003);

    Watson? As in the famous Watson of Watson-Crick?

  21. stcordova: The preface shows some of the things I’ve posted about at TSZ in the face of the usual litany of “Sal is clueless, confused,” blah blah blah.

    I don’t see the part where epigenetic changes are passed on to future generations.

    Is it in another chapter?

  22. Regarding Henikoff’s criticism of the New Yorker article:

    In no case that I recall is there an example of a change in gene expression that can be attributed to histone hyperacetylation to the exclusion of non-histone substrates, of which many have been identified.

    Mincing words, Steve? Of course something has to modify the histones.

    Btw, it’s not always a transcription factor that modifies the histones. A key feature of transcription factors is the recruitment of RNA polymerases, but many histone modifying complexes don’t immediately recruit RNA polymerases such as the Polycomb Repressive Complex PRC2 which methylates H3K27 (H3K27 mentioned in Shelley Berger’s paper — the H3K27 acetylation may block PRC2 methylation).

    Steve’s claim of transcription factors being at the top of the epigenetic hierarchy is not a hard and fast rule. The hierarchy model is probably not the best way to describe things. Witness this study on how Royal Jelly makes a bee a Queen vs. a worker!

    Histone deacetylase inhibitor activity in royal jelly might facilitate caste switching in bees.

    Spannhoff A1, Kim YK, Raynal NJ, Gharibyan V, Su MB, Zhou YY, Li J, Castellano S, Sbardella G, Issa JP, Bedford MT.

    Worker and queen bees are genetically indistinguishable. However, queen bees are fertile, larger and have a longer lifespan than their female worker counterparts. Differential feeding of larvae with royal jelly controls this caste switching. There is emerging evidence that the queen-bee phenotype is driven by epigenetic mechanisms. In this study, we show that royal jelly–the secretion produced by the hypopharyngeal and mandibular glands of worker bees–has histone deacetylase inhibitor (HDACi) activity. A fatty acid, (E)-10-hydroxy-2-decenoic acid (10HDA), which accounts for up to 5% of royal jelly, harbours this HDACi activity. Furthermore, 10HDA can reactivate the expression of epigenetically silenced genes in mammalian cells. Thus, the epigenetic regulation of queen-bee development is probably driven, in part, by HDACi activity in royal jelly.
    …..
    10HDA has several pharmacological activities, including antitumour activity (Townsend et al, 1959) and inhibitory effects on vascular endothelial growth factor‐induced angiogenesis (Izuta et al, 2009). Interestingly, valproic acid (a known HDACi) is an inhibitor of angiogenesis (Hrebackova et al, 2010) and several HDACis are used in cancer treatment (Beumer & Tawbi, 2010). Furthermore, neural stem‐cell differentiation into neurons is stimulated by 10HDA (Hattori et al, 2007), a phenomenon that is also observed using TSA (Balasubramaniyan et al, 2006), sodium butyrate (Yao et al, 2010) and valproic acid (Yu et al, 2009). Thus, many of the reported pharmacological activities of 10HDA might be due to its ability to inhibit HDACs.

    http://embor.embopress.org/content/12/3/238.long

    And to Henikoff’s other uncharitable claim:

    And when it came to mentioning actual evidence for phenotypic specification and memory, he cited the Yamanaka factors, seeming not to realize that these are transcription factors, not the etching of marks on histones or DNA, or enzymes responsible for these modifications, or anything else about DNA packaging proteins or their modifications. Mukherjee seemed not to realize that transcription factors occupy the top of the hierarchy of epigenetic information, that this has been widely accepted in the broader chromatin field, and that histone modifications at most act as cogs in the machinery that enforces the often complex programs specified by the binding of transcription factors.

    Oh really?

    Henikoff fails to mention only the 1% success rate of transcription factor induced pluripotency, thus failing to mention the 99% unknown as to why it fails. It shown that it is because there epigenome isn’t completely controlled by transcription factors!

    There is a chapter from Allis textbook that is free online that is relevant. It’s not as simplistic as Henikoff insinuates. It seems to me, Henikoff is just trying to insult the author of the New Yorker article.

    The efficiency of reprogramming from somatic cells to iPS cells is generally <1%. This suggests that not only are the reprogramming factors important in triggering changes, but so are the subsequent stochastic events required to continue the reprogramming process. Because no major differences in the genomic sequences between the original cells and reprogrammed iPS cells have been observed, changes in the epigenetic status, such as by DNA methylation and histone modification, seem to be the critical events for reprogramming. In fact, the use of small-molecule compounds that inhibit histone deacetylase, thereby increasing overall chromatin acetylation levels, can improve the reprogramming efficiency. During reprogramming, silencing of somatic cell genes and reactivation of pluripotent stem cell–expressed genes have been observed. Although these changes are clearly linked to epigenetic statuses, their mechanisms and driving force are still unclear. The generation of iPS cells provides a good model and tool for understanding the epigenetic changes initiated by transcription factors. In addition, iPS cell technology is currently being used for research both as a source of stem cells for therapeutic use and as a tool for studying pathological processes.

    http://cshperspectives.cshlp.org/content/6/2/a018606.full

  23. Sal,

    When did regulation by transcription factors binding to promoters stop being within the definition of “epigenetic”? When was it ever a thing that insect castes were supposed to be due to genetic differences? Or is it perhaps important that the part you didn’t put in bold talks about “the epigenetic changes initiated by transcription factors”, which suggests you might be misunderstanding something?

  24. Regarding the effect of Royal Jelly on creating Queen Bees — it refutes Henikoff and Ptachne’s assertions that transcription factors have primacy on the epigenome. This is like trying to argue whether the spark plugs or wheels have primacy in the functioning of a car.

    There is more than one route to modifying the histones and DNA methylome, it’s not just transcription factors. In the case of the Queen Bee it appears 10HDA (which is not a transcription factor) affects histone modifications critical to making the Queen Bee. Ergo, Henikoff is avoiding experimental evidence.

    Regarding pluripotency, it seems there are other influences to pluripotency than just the Yanakama factors. It seems micro RNAs are important, and if so this refutes Henikoff’s hierarchical model where transcription factors have primacy:

    MicroRNAs, along with transcription factors, produce homogenous iPS cell colonies from mouse fibroblasts

    For the first time, microRNAs have been used to facilitate reprogramming. MicroRNAs — short stretches of nucleotides that can suppress translation of certain genes — are one of several strategies being pursued in the search for the best techniques to create induced pluripotent stem cells, a type of cell that behaves like embryonic stem cells but isn’t derived from embryos and has vast implications for cell therapy, drug discovery and disease modelling. So far, all techniques to reprogram cells have required the insertion of pluripotency genes, which either directly alters a cell’s DNA or creates the potential for the alteration to occur. Recently, several labs have made headway using small molecules instead of genes1. Now a team led by Robert Blelloch at the University of California, San Francisco shows that microRNAs are another potential tool for reprogramming without gene insertion2.

    “I certainly think that replacing the other transcription factors, alone and in combinations, [with] miRNAs is the next logical step,” says Louise Laurent of the University of California, San Diego. She notes that another group had previously used microRNAs (miRNAs) to reprogram cancer cells,3 but because they used cancer cells, it was unclear whether the strategy would work in normal cells. All this, and the small molecule work, “make it very likely that reprogramming can ultimately be achieved using relatively facile methods” that avoid any sort of genetic manipulations, says Laurent

    http://www.nature.com/stemcells/2009/0904/090423/full/stemcells.2009.62.html

  25. you have implied that your professors agree with you.

    What do you mean? I have to agree with them, not the other way around.

    I posted something like the following diagram straight from peer review and shown in class slides and totally relevant to this discussion. You have a problem with it? Instead I saw a never ending litany of “Sal doesn’t understand, this is irrelevant, you haven’t supported your claims….” blah blah blah.

    I said epigenome is like RAM, hundreds of comments protesting my claim, but then I supported it with pages from the stem cell handbook. Has that caused retractions by my critics now that I supported my point with mainstream literature?

    Well this stuff is quite relevant, especially to the OP. Why should this diagram be disagreeable? It came from here:

    http://www.nature.com/ni/journal/v11/n7/full/ni0710-565.html?message-global=remove

    Epigenetics studies the phenotypes that are born from past experiences and are kept for life.

  26. FwIw, all I think the NYer article needed was an acknowledgment that there are some current controversies and that the author’s statements on those issues shouldn’t be taken as a recitation of a scientific consensus. I take it none of the top contending positions make iD more or less likely or plausible. If that’s so, as many here seem to believe, maybe Sal’s suspicion that money is playing a role here (rather than religious ideology) makes sense.

  27. The author was out to unch in suggesting that any of this was new or that any of it had anything to do with evolution.

  28. Allan Miller responds to me:

    stcordova,

    Epigenetics no longer in the literature even necessarily implies inheritance

    It never did.

    Yes it did! See:

    http://www.epigenome.eu/en/1,1,0

    In the 21st century you will most commonly find epigenetics defined as ‘the study of heritable changes in genome function that occur without a change in DNA sequence‘.

    NIH Roadmap Epigenomics (300 million dollar budget, with that amount of money they can set the standard for the definition)

    http://www.roadmapepigenomics.org/overview

    Overview of the Roadmap Epigenomics Project

    Epigenetics is an emerging frontier of science that involves the study of changes in the regulation of gene activity and expression that are not dependent on gene sequence.

    For purposes of this program, epigenetics refers to both heritable changes in gene activity and expression (in the progeny of cells or of individuals) and also stable, long-term alterations in the transcriptional potential of a cell that are not necessarily heritable.

    What is “new” is the improved understanding of the mechanisms of non-DNA memory that enables Queen Bees that have the same DNA as worker bees to become queens. Allis and friends helped bring a little understanding into the mechanisms.

  29. Regarding the Carpenter Ants in the New Yorker article, here is a 2015 press release from UPENN:

    http://www.uphs.upenn.edu/news/News_Releases/2015/12/berger/


    It’s All About the Histone

    The almost decade-long collaboration between the Berger, Liebig, and Reinberg labs, supported by the Howard Hughes Medical Institute, blends molecular biology with observations of animal behavior to understand how caste-based differences arise in ants.

    Ants, as well as termites, and some bees and wasps, are eusocial (or “truly social”) species. Previous work suggested that histone acetylation could create dramatic differences in gene expression between genetically identical individuals, contributing to the physical differences in body size and reproductive ability between ant castes.

    The current study expands on this narrative by showing that caste behaviors are also regulated by epigenetic changes in histone acetylation. To do so, the team used the fact that chromatin structure — the coiling of the DNA around histone proteins — can be altered by the addition of acetyl groups, which ultimately changes the compaction of the genome. Modifications like histone acetylation allow DNA to uncoil, whereas others cause DNA to become tightly compact and inaccessible to the proteins that regulate gene expression.
    ….

    One can’t fault the author of the New Yorker for misunderstanding or misreporting, he stated was is accepted as science in some respectable quarters. Obviously some other scientists took exception to the claims. It doesn’t make the New Yorker article’s claims untrue.

    I’ve stated my opinion, Henikoff is demonstrably wrong, and one Nobelist who said there is no epigenetic code is not even acknowledging the phrase “epigenetic code” is a hypothesis that is on the table.

    There is something going on that doesn’t strike me as wholesome in the criticisms of the New Yorker article. Why go after the article when then go after the actual researchers like Shelly Berger?

    Btw, let’s follow the money trail as posted on that press release:

    The research was supported by a Howard Hughes Medical Institute Collaborative Innovation Award (2009005), an NIH training grant (T32HD083185) and an NIH New Innovator Award (DP2MH107055).

  30. stcordova,

    I don’t have a problem with these guys disagreeing with the article, because they are qualified, which is more than I can say for Coyne.

    Ha bloody ha! Instant-expert-on-everything Sal Cordova won’t take Coyne’s criticisms because he’s not qualified! Chortle. Where’s me coffee.

  31. stcordova,

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

    Me: It never did.

    Sal: Yes it did! See:

    http://www.epigenome.eu/en/1,1,0

    In the 21st century you will most commonly find epigenetics defined as ‘the study of heritable changes in genome function that occur without a change in DNA sequence‘.

    G’grief, the very first sentence reads: “Conrad Waddington (1905-1975) is often credited with coining the term epigenetics in 1942 as “the branch of biology which studies the causal interactions between genes and their products, which bring the phenotype into being””

    No mention of inheritance. So now people have chosen to ADD inheritance, and you have decided it “no longer necessarily implies it!”. Start at the beginning, and you may see why I said what I did. It never did necessarily imply inheritance, notwithstanding the emendment on a blogsite that (wrongly IMO) restricts the topic to heritable changes in expression ‘in the 21st Century’.

  32. stcordova,

    ENCODE has helped uncover this layer and explicitly used at least one of Allis’ experimental techniques (ChIA-PET), and it doesn’t sit well with Graur:

    If ENCODE is right, evolution is wrong.

    About junk DNA, not about the use or validity of ChIA-PET!

  33. As with his choice of religion, it is Fortunate Indeed that Sal happened upon professors who are on the ‘right’ side of every debate!

  34. walto: FwIw, all I think the NYer article needed was an acknowledgment that there are some current controversies and that the author’s statements on those issues shouldn’t be taken as a recitation of a scientific consensus

    Doesn’t a “serious” magazine like the New Yorker have to do more than simply say this article only presents one side of the story? For example, what if the article came out in favor of homeopathic medicine or said that cold fusion was about to become mainstream science? Would it be enough to say this article does not present the scientific consensus?

    However, unlike those two examples, I understand that there is a real scientific controversy about the extent and reality of “epigenetic inheritance”. But, as far as I can tell, only a (small?) minority of informed scientists believe it has more than short term effects.

    The article was flawed because it did not make that clear and because it did not provide the arguments of the scientific majority.

    ETA: In case anyone missed it, the second post from Coyne is the unpublished New Yorker letter by Mark Ptashne and John Greally which provides a point-by-point refutation of the original New Yorker article.

    Mukherjee has replied to it, I understand, but I have not seen his reply. I’d be interested to know if he attempts to address the science or simply stays with making excuses due to the limitations of publishing in the popular press.

  35. Coyne is not alone, and while he published the point by point analysis, he didn’t write it.

    The thing that ticks off biologists is the New Yorker article ignores 50 years of research and presents epigenetics as some wonderful new idea.

    That, plus the suggestion, barely qualified, that it might provide a wormhole for Lysenko-ian inheritance. All in all, it’s barely above the coffee enemas cure cancer level of science reporting. Just dressed up in a New Yorker quality tuxedo.

    Sal needs to take another look at bees and royal jelly.

  36. Allan Miller:
    stcordova,
    Ha bloody ha! Instant-expert-on-everything Sal Cordova won’t take Coyne’s criticisms because he’s not qualified! Chortle. Where’s me coffee.

    Coyne didn’t write the bloody criticism. He published it.

  37. stcordova:

    There is something going on that doesn’t strike me as wholesome in the criticisms of the New Yorker article.Why go after the article when then go after the actual researchers like Shelly Berger?

    The article was flawed because it was poor science journalism. I expect articles about scientific controversies to first be about an actual scientific controversy, and then to explain both sides of the controversy and to be clear on what the majority of informed scientists currently believe.

    What do you think of the point-by-point refutation of the science in the article presented in the second Coyne post?. If you have time and are interested in doing so, I’d welcome an attempt to address its points, preferably in your own words (since I have little background in this area and often don’t understand the relevance of the large sections of text you sometimes quote).

  38. stcordova,

    I said epigenome is like RAM, hundreds of comments protesting my claim, but then I supported it with pages from the stem cell handbook. Has that caused retractions by my critics now that I supported my point with mainstream literature?

    An analogy is made no better (or worse) by being placed in the mainstream literature. Analogies serve a pedagological purpose; you are trying to spin it into something which in itself has major scientific import. It doesn’t. Science is not advanced one iota by saying ‘it’s like RAM/ROM’.

    What’s important is (for example) methylation and demethylation – mechanisms and consequences. The fact that this might strike one as ‘a bit like’ flipping a bit on a silicon chip is completely unimportant. Pasting diagram after diagram, quote after quote that ‘agrees with you’ does nothing but service your own ego.

  39. BruceS,

    ([…] I have little background in this area and don’t often understand the relevance of the large sections of text you sometimes quote)

    You’re not the only one, heh heh!

  40. What interests me, in the quotes collected by Coyne, is the view of numerous experts that various small-molecule modifications do not support the view of these marks contributing to a system of epigenetic ‘memory’. Such marks are downstream of genetically specified transcription factors in all cases so far elucidated.

    Whatever percentage of the total that might be, it requires at least one concrete counterexample before we can move on from ‘methylation is a-bit-like-like RAM’ to ‘methylation is-a-form-of RAM’.

  41. As pointed out, analogies are teaching aids. One does not reason from analogy. Analogies have no entailments.

    Map. Territory.

  42. petrushka:
    As pointed out, analogies are teaching aids. One does not reason from analogy. Analogies have no entailments.

    Map. Territory.

    Asking for ‘entailments’ is asking for too much, I think. There’s a sense in which no empirical entailments are legitimate. If an analogy is good, it may be fruitfully illustrative. That’s all that can be expected of it, but it’s not nothing.

  43. BruceS,

    I don’t disagree with any of your post, but it’s kind of a matter of degree IMO. I too would like to see the response. And if it’s true that the NYer is refusing to print critical letters on the article, that strikes me as completely inappropriate (as well as couinter-productive from their own point of view, since it makes them look chicken).

  44. walto: it may be fruitfully illustrative. That’s all that can be expected of it, but it’s not nothing.

    The point is that you can not prove anything about reality by reasoning from the implied entailments of an analogy.

    If something in biology resembles something in the realm of digital computers, very well. It may pry loose some brain cells and enable thinking about processes.
    But drawing conclusions about chemistry or biology from such analogies is crankery.

  45. petrushka: The point is that you can not prove anything about reality by reasoning from the implied entailments of an analogy.

    If something in biology resembles something in the realm of digital computers, very well. It may pry loose some brain cells and enable thinking about processes.
    But drawing conclusions about chemistry or biology from such analogies is crankery.

    I agree with that (and note that sausages flinch and squeal when tossed on a hot grill). My point was that ‘proofs’ are tough to come by using ANY means.

  46. I’m not thinking about formal proofs. I’m thinking of heuristics.

    Thinking about genomes as like computer programs leads one off the tracks.

    Computer instructions are strict and formally defined. Chemistry is messy and fuzzy.

    Genetic “instructions” are more like tendencies than they are like formal causes.

Leave a Reply