Name It / Claim It: Epigenetics Now Just Another Evolutionary Mechanism

_{Cornelius Hunter
April 19, 2016

Epigenetics, Intelligent Design

1}_{Categories
Epigenetics
Intelligent Design}

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It is often said that all truth passes through three stages. First, it is ridiculed. Second, it is violently opposed. Third, it is accepted as being self-evident. And so it is with epigenetics which evolutionists opposed and blackballed for a century before finally appropriating it as just another mode of evolutionary change. (see here, here, andhere for more discussion of this history of misdirections regarding Lamarckism and epigenetics). Here is an example of evolutionists, after a century of denial and rejection, claiming epigenetics as their own. Read more

Comments

Zachriel: Embryogenesis is essentially a single cascade,(...)
Thank you for this clarification. To clarify further: is it your position that this cascade — the embryo development — is controlled by a genetic program? - - - You again fail to respond to my question about Venter's Syn 3.0, which I take as an admission that its compatibility with an existing epigenome poses a conundrum for evolutionary theory.Origenes_{April 27, 2016
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Origenes: It is exactly this difference that eludes Zachriel’s understanding. In fact, we have been discussing the whole organism and embryogenesis. With embryogenesis, the process is via a cascade, not a step-by-step instruction manual. It's only by looking at the whole that the process can be understood. Origenes: Or perhaps he holds that there is one uninterrupted cascade? Embryogenesis is essentially a single cascade, however, one that is compounded by complexity. Origenes: These membrane targets provide crucial information—spatial coordinates—for embryological development. Sure. So? Origenes: Even so, my question, still stands. Z: Embryogenesis is a cascade. O: Are you saying that there is one uninterrupted cascade till death ... ? Z: Huh? We were discussing embryogenesis. O: My question still stands. Origenes: ... with no exact beginning? Embryogenesis begins when the egg is fertilized. Origenes: Is an organism something winding down like a wind-up clock? Aging is a different question, but it's clear that metazoan organisms do wind down; that is, they age; with telomeres being the clock.Zachriel_{April 26, 2016
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Zachriel: While we don’t know everything about embryonic development, the mapping of many of the basic signalings involved have been worked out, e.g. BMP4 involvement in dorsal-ventral asymmetry.
Here an example of non-basic signalings:
Another important source of epigenetic information resides in the two-dimensional patterns of proteins in cell membranes.18 When messenger RNAs are transcribed, their protein products must be transported to the proper locations in embryonic cells in order to function properly. Directed transport involves the cytoskeleton, but it also depends on spatially localized targets in the membrane that are in place before transport occurs. Developmental biologists have shown that these membrane patterns play a crucial role in the embryological development of fruit flies. Membrane Targets For example, early embryo development in the fruit fly Drosophila melanogaster requires the regulatory molecules Bicoid and Nanos (among others). The former is required for anterior (head) development, and the latter is required for posterior (tail) development.19 In the early stages of embryological development, nurse cells pump Bicoid and Nanos RNAs into the egg. (Nurse cells provide the cell that will become the egg—known as the oocyte—and the embryo with maternally encoded messenger RNAs and proteins.) Cytoskeletal arrays then transport these RNAs through the oocyte, where they become attached to specified targets on the inner surface of the egg.20 Once in their proper place—but only then—Bicoid and Nanos play critical roles in organizing the head-to-tail axis of the developing fruit fly. They do this by forming two gradients (or differential concentrations), one with Bicoid protein most concentrated at the anterior end and another with Nanos protein most concentrated at the posterior end. Insofar as both of these molecules are RNAs—that is, gene products—genetic information plays an important role in this process. Even so, the information contained in the bicoid and nanos genes does not by itself ensure the proper function of the RNAs and proteins for which the genes code. Instead, preexisting membrane targets, already positioned on the inside surface of the egg cell, determine where these molecules will attach and how they will function. These membrane targets provide crucial information—spatial coordinates—for embryological development. [S.Meyer, 'Darwin's Doubt', Ch. 14 The Epigenetic Revolution]
Origenes_{April 26, 2016
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Zachriel,
Gpuccio: So, there is a big differences between understanding specific parts of biological interactions, and understanding the whole picture, and how it is controlled.

Zachriel: .....
It is exactly this difference that eludes Zachriel's understanding. Or perhaps he holds that there is one uninterrupted cascade? Whatever the case may be, he doesn't want to say it.
Zachriel:
Origenes: As per usual, you speak in riddles, instead of clearly stating what you mean. So, I have to ask some more questions in order to get some clarity (sigh). Here goes … are you saying that there is one uninterrupted cascade till death with no exact beginning? Is an organism something winding down like a wind-up clock? Is that your concept?
We were discussing embryonic development, especially with regards to metazoa.
Even so, my question, still stands. And so does my question about the evolutionary explanation for the compatibility of an existing epigenome with Venter’s Syn 3.0Origenes_{April 26, 2016
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gpuccio: That dose not appear to be a branching process The evidence is that it is a branching process. Development starts with basic differentiations that are inherited from very ancient ancestors; these are then successively modified during development. Origenes: are you saying that there is one uninterrupted cascade till death with no exact beginning? We were discussing embryonic development, especially with regards to metazoa.Zachriel_{April 25, 2016
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Zachriel:
Origenes: What controls when, where and how much of the signal that starts off a cascade?
One of the earliest is the differentiation between dorsal and ventral.
As per usual, you speak in riddles, instead of clearly stating what you mean. So, I have to ask some more questions in order to get some clarity (sigh). Here goes ... are you saying that there is one uninterrupted cascade till death with no exact beginning? Is an organism something winding down like a wind-up clock? Is that your concept?
Zachriel:
Origenes: Venter’s Syn 3.0 is a heavily modified ‘new’ genome which is compatible with an existing epigenome. What is the evolutionary explanation for the compatibility?
Still don’t know what you’re trying to say. It’s a stripped down genome. Why wouldn’t it be compatible?
The genome was not only stripped down, but also tidied up by reordering the remaining genes. Still the unmodified existing epigenome is able to work with the heavily modified genome. Why is that? Wouldn't you expect some cascade hiccups instead? What is the evolutionary explanation for the compatibility?Origenes_{April 25, 2016
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Zachriel: If information is stored, it is written. You can call it a set of instructions or not. The fact remains that you need complex configurations which give a specific result. If the result is a specific transcriptome and proteome in a differentiated cell which has definite functions, and a definite place in the body plan, then you need all those specific configurations that will make the stem cell become that differentiated cell at the right time and in the right place. Those configurations can be in the sequence of protein coding genes, or in non coding DNA, or in cytoplasmic components, or anywhere else: for what we know, as I have tried to say, a lot of different "signals", at various levels, are necessary and must be integrated for differentiation to happen. And remember, many different kinds of differentiation have to happen from the same original cell, at different time and space patterns. That dose not appear to be a branching process, rather the development of a carefully orchestrated program, whose complexity we are not yet able to understand. It's irrelevant that the information is written in what you would recognize as a "set of instructions" or not: the simple truth is that it acts as a set of instructions, but we don't know how it is written.gpuccio_{April 25, 2016
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gpuccio, image a collection of parts bins from which nothing is ever constructed, because there are no instructions for putting the parts to use. The cell manufactures the parts, but never "knows" what do do with them. they all "just happen" to function together. Pure magic.Mung_{April 25, 2016
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gpuccio: The only problem is that information can be “unfolded” only if it is written somewhere. That's a mathematical claim. The information has to be stored somehow, but it doesn't have to be stored as a written set of instructions. It's like how an oak tree grows. There's no instruction set about which branch to put where. Rather, there's a branching process. Origenes: What controls when, where and how much of the signal that starts off a cascade? One of the earliest is the differentiation between dorsal and ventral. Origenes: Venter’s Syn 3.0 is a heavily modified ‘new’ genome which is compatible with an existing epigenome. What is the evolutionary explanation for the compatibility? Still don't know what you're trying to say. It's a stripped down genome. Why wouldn't it be compatible?Zachriel_{April 25, 2016
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Mung: "We call that evolution." Great! :)gpuccio_{April 25, 2016
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Zachriel:
Origenes: Sure, but the question is: what controls when, where and how much of that “one signal”?
The previous signal. That’s what is meant by a cascade.
What controls when, where and how much of the signal that starts off a cascade?
Zachriel:
Origenes: How did natural selection prepare an existing epigenome for a new genome — modified by Venter?
Don’t understand your question.
Venter’s Syn 3.0 is a heavily modified ‘new’ genome which is compatible with an existing epigenome. What is the evolutionary explanation for the compatibility?Origenes_{April 25, 2016
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That’s exactly what happens in human software too. The only problem is that information can be “unfolded” only if it is written somewhere. We call that evolution. :)Mung_{April 25, 2016
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Zachriel: "You seem to think that the information is stored in a human-like fashion, with the events all written down in order somewhere." No, I don't think that. I simply think that the information is written somewhere and in some form, and that we don't know where it is. Wherever it is, it requires specific configurations of bits, like any form of information. "Rather, the information is unfolded in a cascade of events, each event triggering other events." That's exactly what happens in human software too. The only problem is that information can be "unfolded" only if it is written somewhere. Moreover, you know well that complex software requires not only sequential events, but also logical decisions, error checking, robustness, and so on. All those things require specific configurations of bits, IOWs, information, written somewhere in some form. Take, for example, the case of Induced pluripotent stem cells. We know that we can obtain them by adding a few transcription factors. Does that mean that we understand the process of de-differentiation? No. We just add the TFs, and wait. Time goes by (a few of weeks, usually), and with some luck a few of those precious stem cells are obtained. But we don't really know how that happens. So, there is a big differences between understanding specific parts of biological interactions, and understanding the whole picture, and how it is controlled.gpuccio_{April 25, 2016
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gpuccio: You say: another signal. OK, but as I said all signals are potentially there, in the genome. Choosing the correct signal in the correct cell at the correct time requires information. IOWs, epigenetic information is not so much in the signals themselves, but rather in the configuration of signals in space and time. You seem to think that the information is stored in a human-like fashion, with the events all written down in order somewhere. That's not how it works. Rather, the information is unfolded in a cascade of events, each event triggering other events.Zachriel_{April 25, 2016
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gpuccio: “Simple structures”? There is nothing simple in the zygote, or in stem cells. We're not referring to the individual cells, but to their differences, the differences which make up the metazoan bauplan; and while nothing is ever quite so simple in biology, the appellation of simple is reasonably applied to a differentiation that starts with a single cell type, then into two or three cell types and simple symmetries, then into many cells types with more complex relationships. gpuccio: Whatever you can say about trees, it is clear that just a sequence of genes or non coding genes which is common to all the cells in the organism is not likely to explain the ordered and specific development of different functional cell types, according to a body plan, unless specific configurations of information, in the sequence or elsewhere, are able to control the process. The information is unfolded in the cascade of events.Zachriel_{April 25, 2016
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Zachriel: "What we do know is that the developing organism starts with a few simple structures, which are then modified in increasing levels of specificity and diversity, and that this occurs through a cascade of signals." I don't understand what you mean. "Simple structures"? There is nothing simple in the zygote, or in stem cells. They are not "simpler" than a differentiated cell, only different. Indeed, in stem cells, at least at the level of histone code, most genes are in a double condition, of contemporary activation and inhibition. Differentiation usually implies the achievement of the final activated or repressed state by the appropriate genes for the cell type which is being generated. The problem, again, is: how is the decision about the correct development of "specificity and diversity" initiated and maintained, in different cells with different destinies? How are those different choices integrated into the correct body and tissue plan? Whatever you can say about trees, it is clear that just a sequence of genes or non coding genes which is common to all the cells in the organism is not likely to explain the ordered and specific development of different functional cell types, according to a body plan, unless specific configurations of information, in the sequence or elsewhere, are able to control the process. Can you say what those specific configurations are? How they work? IOWs, the question is not: is BMP4 a signal which is necessary to some specific differentiation process? but rather: why is that signal initiated in some specific cell, place and time? You say: another signal. OK, but as I said all signals are potentially there, in the genome. Choosing the correct signal in the correct cell at the correct time requires information. IOWs, epigenetic information is not so much in the signals themselves, but rather in the configuration of signals in space and time.gpuccio_{April 25, 2016
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Suppose that science can prove quantum entanglement of two particles inside the cell. As I understand it, such proof could be based on two empirical findings: 1. The coordinated spin of the two particles. 2. No conceivable local mechanism to account for the coordination. Now consider numerous entangled particles encapsulated by a cell membrane. However, in this case, “entangled” does not pertain to something banally simple as spin, but to homeostasis instead. That is, all the particles inside the cell are coherently aimed at keeping the cell alive — let’s call it 'homeostatic entanglement'. With homeostatic entanglement, just as with quantum entanglement like coordinated spin, we witness a coordinated directiveness of the particles involved. And just as with quantum entanglement there is no conceivable local mechanism to account for overall homeostatic entanglement. One may object by saying: but unlike spin we cannot scientifically measure something like “coherent directiveness towards homeostasis.” But I would reply that the health of the organism offers excellent opportunity for scientific measurements.Origenes_{April 25, 2016
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Origenes: Sure, but the question is: what controls when, where and how much of that “one signal”? The previous signal. That's what is meant by a cascade. gpuccio: Epigenetic regulations are not trees, they are parallel and integrated levels of intervention. Development unfolds in a treelike pattern. gpuccio: Each different tissue cell implements completely different groups of “cascades”. That's right. It's treelike. A few tissue types further differentiate. gpuccio: And please, consider the most important level of all (probably): the network of trascription factors. They do not work in cascade, but rather combinatorially. There is a basic structure as the zygote forms, then these structures are then modified, then those more detailed structures are further modified. This doesn't preclude that the final network may not be treelike. gpuccio: Do you really believe that having notions of how some isolated cascade works means understanding the general picture? What we do know is that the developing organism starts with a few simple structures, which are then modified in increasing levels of specificity and diversity, and that this occurs through a cascade of signals. gpuccio: This is about the combinatorial nature of TFs That's nice, but doesn't address the point; development occurring through a cascade of signals doesn't preclude a complex non-treelike network from forming. Origenes: How did natural selection prepare an existing epigenome for a new genome — modified by Venter? Don't understand your question.Zachriel_{April 25, 2016
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Dionisio: Very good contribution! And thank you for describing so well, at #39, those feelings which are very much my feelings too. :)gpuccio_{April 25, 2016
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gpuccio @33 @34 Very interesting reference links. Thank you.Dionisio_{April 24, 2016
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Origenes @30 Excellent question. Yes, at the core of it all we see lots of spatiotemporal decisions that seem to be choreographically in synch despite a very noisy stochastic environment with such an amazing robustness that defies our imagination. On one occasion while having lunch with a biology researcher who was telling me about his work, he suddenly paused and asked me if didn't like the food, suggesting we could order something else. I had not even touched my silverware yet, because my mind was trying to understand and imagine the amazing things he was describing about his research. Bottom line there was nothing wrong with the delicious food in that restaurant. It was all the professor's fault! :) Obviously he laughed out loud when I told him that. :) He said he wished his doc/post-doc students would give that kind of focused attention to his explanations. :) Well, doc and post-doc students have seen and heard much of what he was saying to me that day, hence they don't fall in the kind of 'awe' trance I was in. :) Besides, those of us who have been extensively and intensively exposed to information-processing systems and have worked on engineering design software development projects can't avoid having our imaginations fly uncontrollably when facing the detailed descriptions of biological systems seen these days in research papers. I have to humbly admit to being in such embarrassing situations on a number of occasions. :) What started as curiosity eventually became fascination and finally turned into an irresistible obsession that keeps me awake because time is very limited but the information we want to learn keeps growing exponentially. It's kind of like the situation experienced by a child left in the middle of a fantastic humongous toy/candy store. One just doesn't want to leave it even for a moment. :) We should motivate and encourage more young students to pursue biology research careers. And we should back any serious initiatives that lead to support the biology researchers who are truly dedicated to the advance of scientific knowledge to the benefit of all people.Dionisio_{April 24, 2016
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Origenes @35 Please, don't take me wrong, but perhaps your question seems a little premature in the sense that first we have to understand exactly how all that stuff works before they can try to figure out how we got it to begin with. As gpuccio mentioned, it doesn't seem like we're quite there yet. Work in progress... stay tuned. :) This is not Lego toys or Mickey Mouse stuff. We're seriously dealing with designed 'complex complexity' superior to any supercomputers or to a B787 / A350 (whichever you prefer) or to anything that we know of. Please, believe me, I'm looking forward, with increasing anticipation, to reading the latest research papers that shed more light on the elaborate molecular and cellular choreographies orchestrated within the biological systems. Biology research labs (both wet and dry) are generating an overwhelming amount of data that gradually is allowing us to get a better idea of the big picture. These seems fascinating times to watch (and support) serious scientific research specially in biology.Dionisio_{April 24, 2016
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#36 error correction: "...continuous from..." should read "...continuous form..." instead. Sorry for any confusion caused by that mistake. BTW, regarding the references to CISC and RISC, please let's note that the main discussions out there deal with comparing the pros/cons of those two main microprocessor architectures, but in any case we can't get away without some kind of fundamental instruction set to support the operating system of your choice or your preferred biological system. I think biological systems are based on a novel kind of CRISC architecture which combines the best of both CISC and RISC designs! :)Dionisio_{April 24, 2016
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gpuccio @31 My pleasure. But all I did was copy/paste what you wrote, so that readers, including some of your 'tough' interlocutors could read it again, but in a continuous from, without interruption, in order to understand the idea of your message correctly. BTW, can't wait to read the 'breakthrough' answers to your questions @32:
Each different tissue cell implements completely different groups of “cascades”. How is that achieved?

Do you really believe that having notions of how some isolated cascade works means understanding the general picture?
Those answers -assuming they're serious- might provoke true scientific headline news all over the scientific media! Lots of folks out there are seriously looking for exactly that. The best app software in the world won't do much outside a well designed operating system with the main regulatory clocks issuing the required impulses at correct intervals to activate the appropriate sets of circuits made of a bunch of interwoven logic gates and the established mechanisms to interpret the different app programs coded with that exact operating system in mind. Let's note that microprocessor architectures could be based on either complex or reduced instruction set computing (CISC or RISC) but in either case we deal with fundamental instruction sets that support the whole operating system (or the elusive biological 'procedure' controllers that obsess gpuccio so much that he keeps reminding us about them over and over again). Unless you take advantage of Xamarin, your software written on Visual Studio for a Windows OS won't do much in an Android or iOS machine. BTW, Xamarin has an important coming event named Evolve16, which proves that some evolution stories could be true at the end of the day. :) Legal Disclaimer: please note that I have no conflict of interest in mentioning Xamarin in my comment. I don't receive any kind of benefits from doing so and I'm not directly associated with Xamarin or MSFT.Dionisio_{April 24, 2016
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Zachriel, one more thing to consider: How did natural selection prepare an existing epigenome for a new genome — modified by Venter?Origenes_{April 24, 2016
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Zachriel: This is about the combinatorial nature of TFs: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2836267/pdf/nihms177825.pdf And, obviously, networks can partially lose control: http://bmcsystbiol.biomedcentral.com/articles/10.1186/1752-0509-6-61gpuccio_{April 24, 2016
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Origenes: "Sure, but the question is: what controls when, where and how much of that “one signal”?" I think we perfectly agree on the main point here! :) The nature of such complex regulation networks eludes our understanding, much more than traditional biochemical cascades (see coagulation) or even classical membrane-to-nucleus signaling pathways (which are already complex enough, see for example this simplified figure for apoptosis: http://www.sabiosciences.com/images/Cellular_Apoptosis_Pathway_680.gif ). But, when we get to the nucleus, and to the network of TFs, the complexity increases exponentially. I have always been fascinated, for example, by the hugely complex interaction network of c-myc, one of the best studied transcription factors. Here is a "simple" figure about that from a paper about macrophages in immune response: The paper: http://journal.frontiersin.org/article/10.3389/fimmu.2014.00422/full The figure: http://www.frontiersin.org/files/Articles/101916/fimmu-05-00422-HTML-r1/image_m/fimmu-05-00422-g003.jpg Simple cascades? Not really!gpuccio_{April 24, 2016
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Zachriel: OK, but here we have lots of different and interconnected and alternative "cascades". And the epigenetic regulation is much more than the individual "cascades" which implement some particular effect. Epigenetic regulations are not trees, they are parallel and integrated levels of intervention. Stem cells exist in a continuous range of states, and in some way they find the correct balance between self renewal and differentiation. And this happens at multiple levels and at various stages, from the zygote down to adult stem cells. Each different tissue cell implements completely different groups of "cascades". How is that achieved? DNA methylation, histone post-translational modifications, chromatin remodeling, non coding RNAs of many different categories, all work in parallel. It is really difficult to understand in each situation what initiates what. Look at the recent thread about RNA-Directed DNA Methylation in plants: long and short non coding RNAs which modify the epigenetic status by DNA methylation! And please, consider the most important level of all (probably): the network of trascription factors. They do not work in cascade, but rather combinatorially. Some of the effects on chromatin status seem t be mediated by a complex of 10 - 15 TFs, or even more, acting together in connection with DNA, enhancers, promoters, and so on. Recent bioinformatic analyses of recent biological data allow to map the genome at multiple levels: the methylation state, the modifications of histones, enchancer and promoter status, 3D structure (TADs), and so on, and each of those levels has definite correspondences with functional states and cell types. Do you really believe that having notions of how some isolated cascade works means understanding the general picture?gpuccio_{April 24, 2016
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Dionisio: Wow! Thank you for working do much and so well on my posts! They look really fine this way. :)gpuccio_{April 24, 2016
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Zachriel:
Gpuccio: Do you really believe that “The signaling is the control”?
That is what signaling cascade means. One signal triggers the next; that is, the effect is the cause of the next event.
Sure, but the question is: what controls when, where and how much of that "one signal"?Origenes_{April 24, 2016
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