The writings and life work of Ed Thorp, professor at MIT, influenced many of my notions of ID (though Thorp and Shannon are not ID proponents). I happened upon a forgotten mathematical paper by Ed Thorp in 1961 in the Proceedings of the National Academy of Sciences that launched his stellar career into Wall Street. If the TSZ regulars are tired of talking and arguing ID, then I offer a link to Thorp’s landmark paper. That 1961 PNAS article consists of a mere three pages. It is terse, and almost shocking in its economy of words and straightforward English. The paper can be downloaded from:
A Favorable Strategy for Twenty One, Proceedings National Academy of Sciences.
Thorp was a colleague of Claude Shannon (founder of information theory, and inventor of the notion of “bit”) at MIT. Thorp managed to publish his theory about blackjack through the sponsorship of Shannon. He was able to scientifically prove his theories in the casinos and Wall Street and went on to make hundreds of millions of dollars through his scientific approach to estimating and profiting from expected value. Thorp was the central figure in the real life stories featured in the book
Fortune’s Formula: The Untold Story of the Scientific Betting System that Beat the Casino’s and Wall Street by William Poundstone.
Poundstone’s book doesn’t actually go into detail what formulas actually work in today’s markets because once something works well, it stops working once everyone else figures it out. Thorp’s only published work on how to make money on Wall Street became obsolete and he had to find new avenues of success with secrets he will take with him to the grave….But for those interested, here is Thorp’s only published book on how to make money on Wall Street. As I said it is now obsolete, but it showcases Thorp’s genius and insight. It used to retail for $300 used on Amazon, but then Thorp offered a PDF copy for free:
BEAT THE MARKET
A Scientific Stock Market System.
So if you want a change of pace from the usual arguments over ID, I offer Thorp’s work and you can skip the rest of what is written below since it is my version of ID inspired by Thorp and Pascal.
Though I had followed Thorp’s work on and off for 10 years, I only recently discovered Thorp’s 1961 article while preparing my own draft of a paper that encapsulates my version of Intelligent Design presented at the Blyth Institute’s “Alternatives to Methodological Naturalism Conference” (AM-NAT 2016). I present to the TSZ readers a draft of a paper that I’m submitting as part of the AM-NAT 2016 conference proceedings. AM-NAT 2016 was a conference organized and mentioned by JohnnyB at TSZ and UD. So if you want to argue ID instead of discuss Thorp’s work, that’s ok too.
I got fascinated by the body of math surrounding expected values partly as a result of Thorp’s work. Because of this body of math, I concluded ID theory has been focused too much on information theory and the 2nd law of thermodynamics, and I’ve argued this is a misguided approach. A more clear cut way to frame the probability arguments is to leverage expected values and the law of large numbers and apply similar mathematical approaches, not the approach laid out by Dembski and his almost intractable conception of specification and CSI.
My approach to the question of ID at the personal and practical level has been more along the lines of Pascal’s wagering ideas than trying to make absolutist assertions about reality. Pascal’s wagering ideas were not limited to the theological questions of heaven and hell, but were originally developed to answer theoretical questions about fair values of wagers in gambling games. His solutions using his notion of “expected value” became foundational in probability and statistics, and the notion of expected (or expectation) values has found its way into the realms of physics, chemistry and finance, etc. I’ve framed ID vs. Naturism debate at a personal and practical level more in terms of what is to be gained if ID is right and what might be lost if ID is wrong and how to move forward in science without formal resolution the question of ID.
In my paper, I focused on a practical (not theological) dimension regarding the NIH’s half-billion dollar research investment into the ENCODE and RoadmapEpigenomics projects. Evolutionary biologist Dan Graur has labeled the ENCODE project leaders “crooks” and “ignormuses” and likened the chief architect of ENCODE, Ewan Birney, to Saddam Hussein. Even money aside, there is an issue of bragging rights as to which group of scientists (ENCODE vs. Gruar) should be praised and which group will have egg on their faces after all the dust settles.
To my surprise, the fight over ENCODE spilled over into a fight over what I thought was a rather innocuous article in the New Yorker that promoted the chromatin-centric viewpoint of the epigenome. I did not realize there was a camp (for lack of a better name, I’ll call them the dinosaurs or the transcription-factor proponents or gene-centrists) that was furious at the chromatin-centrists. ENCODE is not only labeled as promoting an “evolution-free gospel” (verbatim words used by rival scientists in a peer-reviewed publication), but they are also not exactly liked by the gene-centrists for their chromatin-centric viewpoint of the epigenome. Creationists and IDists are more sympathetic to the chromatin-centrists, with the qualification that creationists and IDists in general are more favorable to all forms of non-DNA somatic and transgenerational inheritance mechanisms that may reside outside DNA be it organelle, structural, glycomic or whatever “-omic” inheritance devices that may be out there, not just chromatin based mechanisms.
I’ve qualitatively argued the favorable wager in practical terms is on ENCODE, not on evolutionary theory. Most of the paper is rehash of debates I’ve had here at TSZ, so the material is nothing new. It can be said, my paper is really a product of the debates I’ve had at TSZ. The interactions here have helped provide editorial and technical improvements. The paper is still a draft, the figures and formatting will be cleaned up by the myself, reviewers, and the Blyth Institute before it is published in the AM-NAT 2016 conference proceedings. This draft still has a lot of cleanup needed, so I’m posting it to invite improvements. Some of the material might later be reworked as reading material for the high school home school and/or creationist biology students in college. I don’t consider the paper a professional offering, but a way to codify some of my ideas for later reference.
For those tired of reading and arguing what I’ve posted before and have no inclination to read my paper, I provided a link to Thorp’s paper in the chance it may be of passing interest and a change of pace to some readers in this blog.
But for those interested in my paper, here it is:
Gambler’s Epistemology vs. Insistence on Impractical Naturalism: The Unwitting Half-Billion Dollar Wager by the NIH Against Evolutionary Theory.
ACKNOWLEDGEMENTS
Thanks to all at TSZ who have contributed to the refinement of the ideas in my paper. Thanks to the admins and mods of the skepticalzone hosting my postings. TSZ has been a place where I’ve had the chance to receive critical and editorial feedback on materials I’m publishing in various venues.
PS
I had the opportunity to put in practice some of Thorp’s theory in the casino and so did a group of Christians. Their story is documented in the DvD Holy Rollers. I’m listed in the credits of the Holy Rollers documentary.
Here is the trailer. Featured in the trailer is Pastor Mike and other pastors who were part of the Holy Rollers:
John Harshman,
If this is true it would eliminate and reduce possible regulation mechanisms. Do you have any idea how to test the hypothesis?
So there we have it, it’s a new ad-hoc hypothesis for the genome-size of every species that ever lived and every single one currently in existence. They all have their own unique and vastly different ways to use chromatin packaging! What gibberish.
Yes, I have a problem with that, it is an absurdity when we already have a single explanation (the same basic process) for all of them, its evolution: Stochastic accumulations of junk-DNA over time.
An analogy would be that you are positing a supernatural entity to push around every single atom in a river to explain why the water flows downhill, rather than just all the atoms being affected by gravity.
I don’t know what else to say here than, have fun with that.
Or, in other words, you won’t be bothering to answer those important questions. It’s something somebody else has to do, not you.
You should take your paper to the Discovery Institute and ask them to fund research based on it. From what I hear there is room in the 2017 ID Journals for a few papers yet…
Why? We are talking about a particular gene with very long introns. Some genes could be using introns as part of a regulatory mechanism, and others not. To hypothesize that this particular gene’s very long intron is a junk-intron is not to hypothesize that all introns are junk by definition and that none of them are part of a regulatory process.
Remove (or sigificantly shorten it by editing out most of it) the intron and see how the host cell or host organism does. If it is unaffected in development and behavior, this would indicate the intron is mostly junk.
Rumraket,
I do find myself wondering: ‘what’s the fucking point?’. Common design has equal explanatory power to common descent my arse.
On junk, the observation of a physiological effect on removal does not provide it with a function. Remove the junk from my house and I can get to the front door quicker. But its function is not to slow me down.
stc: “The difference in genome size is probably an indication of how differently the chromatin is used.”
Similarly, the difference in leg length among the human population is probably due to the requirement to fill different lengths of trouser.
Common design has equal explanatory power to common descent if the design is assumed to mimic non-interventionist common descent.
I mean, you can do science with common design in that way, but scientifically it is an entirely useless and meaningless step whose sole purpose is to obscure what the evidence shows. ID’s “contribution” to research.
Glen Davidson
That’s true, but with respect to the intron example, if it could be shown that loss of the large intron results in organisms with lower reproductive success, I’d be willing to say it was a functional intron.
Universal common ancestry (aka Common descent) would have explanatory power if it were mechanically feasible and didn’t require events statistically indistinguishable from miracles. Transitions from prokaryote to eukaryote (which sliceosomal introns, nucleosomes, nucleosome related machinery) are events indistinguishable from miracles.
Like the privileged planet hypothesis, life is designed to help man understand himself. Patterns like this are better than evolutionary conserved, they tell you what species to study to understand the parts of humans. No sense studying non-existent mouse genes to understand humans when the gene you need is in a chicken or zebra fish.
But so many things are remarkably helpful, like the ability to study yeast in order to study eukaryotic genomes. It would be so much harder to understand ourselves if we didn’t have organisms with some properties similar to us. Homology (in Owen’s conception, not Darwin’s) is God’s gift.
Isn’t it so nice we have simple organisms with simple genomic architectures like bacteria that don’t have histones and spliceosomal introns when we were first studying how biological systems work. The gradual ladder to complexity seems God-given to help us realize ourselves and our special place in the universe. We’re a privileged species living on a privileged planet.
Some may complain they don’t feel all that special, but rather cursed. Well according to Christian doctrine we are also cursed in addition to being privileged species living on a privileged planet. That’s one of the reasons I find believable Christian theology as proceeding from the Designer of Life himself.
We have thermophile bacteria that gave us that Nobel Prize winning Polymerase Chain Reaction (PCR) that allows us to sequence DNA. We have homology with creatures with semi-transparent eggs which teach us how the developmental process can work. So nice we can study gill slit development in fish than have to play with human beings to understand the development of homologous structures in us. So nice we can re-engineer rats to test our hypothesis about which genes affect limb development than have to do such stuff on human beings.
And additionally in light of the Muller/Graur mutational load conflict with the results and claims of ENCODE, I find common design optimized for scientific discovery a much more satisfying explanation for the patterns of similarity.
And so far as gather in this discussion over gambler’s epistemology, the only potential loss of assuming evolutionary theory is wrong is the loss of evolutionary theory, not much to worry about how it affects operational and applied science like engineering and medicine. On the other hand if we assumed Graur is right and followed through with it, the ENCODE guys would be pegged as “crooks” (to quote Gruar’s words) and that wouldn’t be good for getting grants for useful medical research — like epigenomic cancer treatments.
This is idiotic. Nobody thinks spliceosomal introns, nucleosomes or any of it mysteriously appeared overnight.
Oh wait, YOU do. Literally, believe it happened by miracle. I cannot facepalm enough.
… you know this how? Did an angel reveal this to you during an epileptic seizure?
What’s so ad-hoc about it if turns out to be true. The way genomes and epigenomes and epitrancriptomes work may not be 100% homologous, and that applies to their size as well.
We won’t find out if we don’t look to see how things work, and the naysaying attitude against thing like ENCODE/RoadmapEpigenomics will slow down the process of actually settling the question. But if you prefer to put money on unresolvable evolutionary phylogenies with dubious medical utility, I guess there must be some place you can donate toward that end. As for me, I sent my $35 annual dollars to the Creation Research Society. 🙂
Sal, you can believe in your hypercycle model if you want. I don’t have a need to disabuse you of it. Yes of course dear, the Earth is the center of the cosmos.
Awesome. Maybe they’ll publish another article claiming there are no transitional fossils.
I don’t know it for sure, but I believe, just like you believe the opposite despite and the fact you don’t know for sure either.
Hence I’ve suggested gambler’s epistemology to resolve the decision making process in how to carry on an enterprise like studying the epigenome. The irony is that even if Gruar’s right, you still think money should be directed to the ENCODE “crooks”, which is the right wager and agrees with the fundamental conclusion of my paper : “bet on ENCODE”!
Rumraket,
I dunno … there is the logical possibiility that other systems have evolved in its presence. It does nothing in itself, but other more recent systems are negatively impacted by its loss. It hasn’t even been co-opted, it just forms part of the environment for other genes.
stcordova,
And yet the timing of the various transitions is entirely in accord with the changes one would expect to accumulate since the split on a ‘naturalistic’ scenario. There is no need to invoke something else to explain the data. That something else must explain hierarchy – and why phylogeneticists can even have a field to work in. These things are provided for free within a descent framework. The only way you can make a common design framework work is to pretend that the patterns don’t exist. To, effectively, jab a needle in thine right eye, since binocular input offends thee.
Pointing to the prokaryote/eukaryote split is classic misdirection. This is one of the few occasions chimaeric organisms appeared. The normal tempo of evolution – that which deals with everything else – accords with gradualism.
This has been investigated rather thoroughly, you know?
stcordova,
So what is it, gradual or sudden? Make your mind up.
stcordova,
Not just any old Polymerase Chain Reaction then.
stcordova,
Yes, you hate Graur. I think we’ve gathered that. And everyone on ENCODE is right about everything, including % functionality.
But there is no conflict between 90% of the genome being [eta: non-]functional and cancer treatments having a potential source anywhere within or outside it. The tools of evolutionary biology, meanwhile, are used in medicine. You know, that thing that doesn’t work and makes no difference.
The following is a section from my paper that just gave me a new idea upon reviewing my own writings. Instead of Behe’s term “Irreducible Complexity” I suggested the notion of “Rube Goldberg Complexity” (which Behe indirectly suggested in his famous book), but upon further thought, I think I’ve got the perfect counter to Charles Darwin’s rhetorical gimmicks: “Unnatural Complexity”. Bwahaha! Natural selection cannot select unnatural complexity. Clever eh? Bwahaha! Unnatural Complexity seems like a better buzzword than Specified Complexity.
Anyway, here is the appendix from my paper on Rube Goldberg Complexity:
And the final appendix:
Comparative methods to the rescue: if intron length were under selection, we would expect less variation in the length of particular introns both within and among species than neutral accumulation of indels would predict. Large indels, in particular, would not be expected to occur at a visible frequency. I don’t know the answer in this particular case, but in my experience introns vary quite a bit in size within taxa.
What we see with stcordova here is the classic creationist move to supposedly find some sort of absolute reason why the evolutionary explanation for a number of facts (evolutionary explanation was proposed in order to explain a number of otherwise inexplicable facts) is wrong, and then to suppose that creationism/ID will be the default.
There is no visible interest in explaining what evolution does by anything meaningful. “Common design” is invoked, but of course where we’ve seen that it is nothing like the slavishly derivative nature of the typical eukaryotic reproductive processes and the evolutionary results that we see from those. There is really no evident interest in the crucial purpose of scientific reasoning at all–explaining phenomena.
Which is why creationism/ID is scientifically dead from the beginning. It only really exists in order to prop up an idea (of design, anyhow) that never explained anything in the first place, except to people whose typical response to the unknown was that some deity was the answer. Evolutionary theory does explain huge amounts of biology, far better than anything else ever proposed, but it doesn’t promise what religion does, hence it must be found to be wanting.
ID can never be science, and evolutionary science can never be religion. Because the two different sides actually want very different things, there never is a meeting of the minds.
Glen Davidson
stcordova,
Why not?
GlenDavidson,
What do you think evolution explains? As a historical science like ID it is an inference explanation. Design has been a competing inference since Darwin. It is certainly a minority view but it is a scientific inference.
One creationist theory, Genetic Entropy, makes a testable prediction about the true evolution of the human genome — that is toward deterioration. That is a testable and falsifiable claim with medical relevance. There are probably some things extensible to ecology and the environment, namely increasing selection pressure by reducing the number natural resources won’t induce emergence of radically novel forms. Selection pressure (as in less human environmental intrusion) has to be alleviated to at least maintain the species we have otherwise the “6th great extinction” will keep going.
Darwin never thought much about what increasing selection pressure will actually do (like starving the food supply), nor about mutation load, nor about gambler’s ruin that relates to drift, etc. etc.
His theory of “Natural Selection” is not what happens in nature. The label is false advertising, it is a rhetorical trick, it is falsified science since it doesn’t agree with experiment and observation where it really counts, namely macro-evolutionary change or anything remotely approaching it.
stcordova,
How long have you been discussing evolution online now? You know that Natural Selection is differential reproduction causally linked to genetic variation, surely? And you say that does not happen?
Here’s another creationist who claims in one breath that creationists agree that microevolution happens and in the next claims that natural selection, the most visible mechanism of phenotypic microevolution, does not. Go figure.
That is why creationism is equivalent to volitional insanity.
John Harshman,
Here is a paper supporting regulatory control of introns. Mikkel seems to agree that there is some regulatory relevance to introns. His proposed experiment would help us to understand this. So if length matters, are the intron’s where length matters but sequence doesn’t junk?
Rumraket,
Thanks for the idea on testing 🙂 So far found this hypothesis:
You need to provide a citation and/or a link. Yes, that would be a useful bit of data. So would be the comparative data I suggest. And I agree that only the genes with extreme amounts of intron sequence are good candidates for such regulation, if there are any.
As for definitions, I think the most useful thing would be to create a third category: junk, bulk-functional, and sequence-functional DNA.
John Harshman,
Mol Biol Evol. 2014 Nov; 31(11): 2879–2889.
Published online 2014 Jul 28. doi: 10.1093/molbev/msu226
PMCID: PMC4209130
Transcript Length Mediates Developmental Timing of Gene Expression Across Drosophila
great idea 🙂
Sal quotes DNA_Jock thus:
And responds:
No. I did not. That is false. My original post included all of Sal’s phrase, to wit :
In English, this sentence is an example of gapping ellipsis, which can be expanded thus without alteration of meaning:
There is ambiguity as to whether the adverb “directly” should be included in the expansion. I gave Sal the benefit of the doubt.
Hence my reaction:
Sal tries to explain
I heartily recommend that you permanently stop extending the implications of anything you read. You keep doing it wrong. OTOH, I have been encouraging you to use your own words, if only because it does reveal your misunderstandings.
While I’m sympathetic to the usage “proteins are made from a direct DNA template” (heck, I used it myself above), in the context of the contrast you are trying to make here, it is not actually true…Lots of “other factors” get in the way of that ‘direct’ relationship – mRNA processing, post-translational modifications (such as formyl glycine) etc. IMO the big difference between the flow of information from DNA to protein and that involved in glycan synthesis (BTW, you should probably distinguish peptidoglycan from glycosoaminoglycan here) is that scientists have a better understanding of the former.
Or, alternatively, your “template” concept is incoherent.Heh.
Well, you were trying to draw that distinction, which is one of degree and of current state of knowledge rather than an absolute, but your sloppy use of language let you down yet again.
No. I just wanted to clarify your meaning: what you in fact said was wrong. What you now claim you wanted to say is merely pointless.
I will respond to this below – saving the best for last, ‘nall.
Insofar as I can decipher that mangled English, yes, I do.
Actually, I can (under certain circumstances). You have both your logic and your facts wrong here.
Let me generalize that statement for you:
X megabytes of
DNAinformation does not a human make. You need CHOPNS, salts, water and a source of energy.Now my favorite:
Yes I do. Emphatically. Why on earth you think your “rebuttals” of my position carry any weight, I cannot imagine. I have been ever so gently (too gently, and too fearful of being seen as “tooting my own horn”) been trying to guide you to the realization that I am familiar with the structural studies that were performed elucidating the nature of “chromatin”.
So when you show me a micrograph of the 30nm fibre I respond
Seriously, Sal, I knew the guy who pioneered this work.
Your response: to accuse me of claiming that it was not chromatin. Not what I wrote. I point this out.
You opine:
I reply:
Oh Sal, I deliberately chose a bad example of a “British man”. I could forgive your missing the point if I had suggested a photo of Winston Churchill, but I picked an Irishman, FFS! Do I really have to spell this out for you? Just because you post a photograph of something (and a fuzzy one at that. Oh, the irony!) it doesn’t mean that it isn’t a fuzzy concept.
Finally, to further prove to me that I am hopelessly wrong about “chromatin” you cite the press release announcing Aaron Klug’s Nobel Prize. Well, your choice of “rebuttal” had me rolling in the aisles.
In truly English style, I replied:
along with a photograph of a bottle of champagne (artfully positioned atop a copy of “A Genetic Switch” by Mark Ptashne. Heh.)
It may have escaped your notice, but said bottle is autographed and dated “Aaron Klug, 18 October 1982”.
Let me translate our interaction into American English.
Sal: “A Nobel Prize was awarded for elucidating some of the structure of chromatin: [link to press release]”
DNA_Jock: “Yes, I’m quite aware of that, seeing as I personally celebrated the announcement by drinking champagne with the winner, and I have the bottle to prove it, you twit.”
By now I really should know better that to try to be subtle with you.
Iff there is such a thing as bulk-functional DNA, which is yet to be established.
Couldn’t read the hand writing on the bottle, I did try to read it.
Subtle? how about not clear at all. Some people are deliberately cryptic, and when what they say isn’t understood from lack of their clarity, they sometimes interpret it to mean they possess superior knowledge that can’t be understood by lesser minds when in fact it was their lack of clarity.
The listing of all the exact components of chromatin constantly changes, but lots of things in biology are dynamic. By that standard lots of biological concepts would be fuzzy starting with the definition of human, so your statement that chromatin is a fuzzy concept isn’t used a lot, it maybe called a fuzzy organelle because it is dynamic and the parts are hard to isolate, but the basic DNA/nucleosome/histone architecture is there, and it is seen in the photograph.
Your bottle photo was one of your comments to me after you got called on a false statement which you’ve not retracted despite being called on it several times. Here is your false comment again:
You said that despite the fact just a few comments earlier I made the distinction and even with the right buzzwords, “somatic” and “transgenerational”, so not only was I right, I was right with some style points to boot:
Then I parsed it out for you since you were unwilling to concede that my statement was indeed making the distinctions you claim I didn’t make. And you responded with even more irrational comments after I parsed the statement out for you in this way:
But even then you would admit to the readers you made a false claim.
Your best comment subsequently was photo of autographed champagne bottle.
I didn’t know I was dealing with varsity. Given you were unwilling to comprehend the implications of a simple phrase:
I didn’t realize you were of such high rank in science that you could get an autographed champagne bottle. Now that you’ve shown me you have a champagne bottle autographed by Klug, I can pat myself on the back even more when I show where you are in error.
I can pat myself on the back and say, “I showed up DNA_jock in debate, and he’s one of those special guys that are so special and brilliant and esteemed in the scientific community that he got an autographed champagne bottle.”
Since the topic of epigenetic inheritance is in the paper, just to clarify, chromatin can be involved in somatic and/or transgenerational epigenetic inheritance. Since DNA_jock, who I didn’t realize was so high in the echelons of science that he could secure an autographed champagne bottle — since someone as smart DNA_jock would apparently have problems if I said something to the effect:
I decided to provide a little more elaboration in the form of a Venn diagram since Venn diagrams are often useful for teaching 2nd graders concepts.
The Venn diagram shows the concept of epigenetic inheritance in general (represented by the blue are) and there are two varieties of epigenetic inheritance, namely “somatic” (in the dark orange bubble) and “transgenerational” (in the light green bubble).
“Somatic epigenetic inheritance” is a conceptual member the set of forms of epigenetic inheritance. “Transgenerational epigenetic inheritance” is also a conceptual member of the set of forms of epigenetic inheritance.
If I said:
It means chromatin can be involved in all forms of epigenetic inheritance whether (1) talking separately about somatic epigenetic inheritance or (2) separately about transgenerational epigenetic inheritance or (3) both forms of epigenetic inheritance.
I’m going the extra mile since it seems that parsing a phrase like this one:
is confusing even to someone accomplished enough to have an autographed champagne bottle.
Over how many generations is this transgenerational epigenetic inheritance involving chromatin stable?
Ooh, don’t ask that, John! For methylation it’s at most a few generations, and the whole notion that that epigenetic mechanism can act like Mendelian inheritance crumbles. As I suspect it would for chromatin configuration too.
In plants where clones don’t have to pass through germline inheritance, the epigenetic marks can stay there a long time across cloned generations.
http://www.sciencedirect.com/science/article/pii/S1874939911000575
For mammals it could depend how one defines inheritance. Many wouldn’t say epigenetic inactivation of the X chromosome in females is inherited even though the same epigenetic marks to inactivate the X-chromosome appears again and again and again across each generation. But that epigenetic mark is “stable” in the sense it keeps reappearing even though it also gets erased in each generation.
The cases for transgenerational chromatin based epigenetic inheritance don’t seem very abundant nor stable (unless one calls stuff like the epigenetic marking involved in things like X-inactivation “heritable”).
John,
If you’re going after the angle of acquired epigenetic characters, I don’t know.
There is the sticking point regarding epigenetic marks that get erased and then re-appear with each generation. These are highly conserved. Definitional debates are endless whether these are truly heritable. One definition would lead to “conserved methylation marks across species” being true but simultaneously not being heritable (since the marks are erased often in the sperm cells only to reappear in the same conserved locations in somatic cells across species.) You can call the epigenetic marks conserved, but Allan Miller and others would get upset if we called such conserved marks across species transgenerationally heritable.
In those cases they don’t seem to be acquired characteristics, their ultimate origin is not known except in some cases where we know that DNA is involved, in some cases it is not known where the exact marking patterns are stored to be later put on the chromatin of various somatic cells.
Regarding transgenerational effects in humans, whether an acquired epigenetic mark is stable or not stable, it is of interest still to the consumers of ENCODE data, particularly the effect of toxins on the epigenomes of grandkids. Suppose grandma was poisoned, even if the toxin isn’t in the grand kids, can the epigenetic effects still be on them?
Transgenerational epigenetic inheritance is of interest to medical researchers even though not necessarily to evolutionary biologists who might think the long term effects are small in the scheme of things.
Any way, a relevant article:
http://www.smithsonianmag.com/innovation/the-toxins-that-affected-your-great-grandparents-could-be-in-your-genes-180947644/?no-ist
One might be tempted to say, “ha, the transgenerational epigenetic marks in mammals aren’t very stable, so it’s not a problem for evolution.”
Well, the problem is more subtle than that, because the somatic chromatin-based epigenetic marks and the machinery that implements them are fairly complex, bewilderingly so. The PRC2 polycomb repression complex that assembles on Chromosome 2 (referenced in my paper) is recruited by the HOTAIR lincRNA originating on Chromosome 12. HOTAIR has to somehow navigate the nuclear complex from Chromsome 12 with no active propulsion and bind to the right site on chromosome 2 — all this to affix a single mark on a histone (the mark called H3K27me).
PRC2 I believe is in fruitflies as well as mammals. The evolution of this stuff doesn’t seem trivial to me. PRC2 is only one of maybe many such complexes. The connections between the proteins of these complexes may involve post-translational modifications (PTMs). Where is the information to specify those PTMs and connections? They don’t seem templated by the DNA.
Unfortuantely chromatin modifications has been equated with epigenetic modifications. Some chromatin modifications happen in the cell-phase, and thus not strictly speaking involved in somatic epigenetic inheritance.
For example, in DNA repair there are lots of chromatin modifications that are mechanically similar to changes in the physical epigenome — one will see chromatin RAM bits being flipped on and off during the repair process.
Hey, that’s a better buzz phrase “chromatin RAM” instead of “epigenetic RAM”. That’s at least more accurate since it doesn’t perpetuate a conflation of chromatin with the epigenome. I may make that amendment in the draft of my paper.
Chromatin provides both epigenetic memory and cell phase memory, chromatin RAM is not solely epigenetic it can also be cellular.
TSZ is wonderful place to refine one’s thinking and get editorial improvements.
stcordova,
So, to sum up.
Transgenerational epigenetic marks can be stable over enough time in clonal plants that they might have some effect on evolution. Not so in animals, though. Epigenetic marks that re-appear in every generation are not transgenerational; they are effects of DNA sequences.
Also, you are laboring under a misapprehension: if epigenetic effects were stable over evolutionary time, they wouldn’t be a problem for evolution. They would merely be another system subject to evolutionary modification, just like the genome.
If you can’t dazzle ’em with brilliance, baffle ’em with bullshit. But have the wit to recognize the difference.
That misses the point, chromatin modification (whether you want to call them epigenetic or whatever) are staggeringly complex. DNA in eukaryotic repair is immensely complex and there is nothing like it in the prokaryotic world.
Depicted below is a simplified diagram of what it takes to do DNA repair in a chromatin architecture. It involves reading, writing, and erasing of the RAM-like histone memories during the repair process, the recruitment of chromatin remodeling complexes, the coordination and management of this entire process, etc.
The macroevolutionary transition from prokaryote to eukaryote has to account for the emergence of these machines and processes with reasonable transitional steps.
Like suggesting phylogenetic reconstructions are satisfying mechanical explanations that the transformation of the prokaryotic architecture to eukaryotic architecture involving chromatin can take place through ordinary and typical events.
To see more detail in the diagram below, one can try looking at the JPEG directly here:
http://d1dvw62tmnyoft.cloudfront.net/content/joces/125/2/249/F1.large.jpg
Or the reader can zoom-in a bit more to see the steps using the powerpoint URL below. I had to download the powerpoint and then zoom to see the details from the URL below:
http://jcs.biologists.org/highwire/powerpoint/1587448
Here is an excerpt from the paper from which the preceding diagram was taken.
Let the reader decide if phylogenetic reconstructions are adequate mechanically detailed explanations for the emergence of the amazing sequence of events involved in chromatin-based DNA repair in Eukaryotes. These are amazing Rube-Goldberg machines that evidence un-natural complexity: