Non-DNA Structural Inheritance

If the DNA codes primarily for proteins and helps regulate protein quantities, then where is the developmental or structural information? I’ve never gotten a straight answer from most evolutionists I’ve encountered, for that matter anyone on planet Earth. Maybe no one really knows. I think Creationist biologist Arthur Jones is right about Non-DNA inheritance.

It would seem, if DNA is mostly about storing the data for protein sequences, as a matter of principle it doesn’t store the structural information for cells and entire bodies. The information is elsewhere, likely in the cytoplasm of the zygote.

DNA locations often have single point of failure locations (like start and stop codon locations). But if large amounts of body plan information is stored in a network topology, it is highly redundant and hence there is not single point of failure if the cytoplasmic basis of heritable information is damaged. Hence it would very hard to “mutate” the body plan information if the information is stored in a network topology.

An example of a network topology in the man-made worlds is BITCOIN which has a redundancy factor in excess of 400 computation centers spread around the globe. If half of the 400 computation centers are destroyed, the BITCOIN collective can still recreate itself and continue functioning. The ability to mutate its basic records without valid transactions is very difficult because of the network topology.

When a network topology is in play, it gives the illusion that because an individual component is dispensable, that the component has no contribution to inheritance. Not so. Destroy enough of the components in the network, and there will be no inheritance. For example, remove the cytoplasm from a cell, and just leave the DNA. The creature will not reproduce! The Gene-centric rather than Whole-Centric view of reproduction is based on the desire for simplistic conceptions and explanations. Thinking in terms of redundant, self-healing network topology is far beyond simplistic thinking or most present day understanding. The claim that DNA codes for everything is naïve. DNA codes for protein sequences, but that is not the same as the description of cell structure or body plans. I’m posting this to invite anyone to show where in the DNA, the totality or even majority of structural information is stored.

The ability to self-heal is evidence network topology is present in multicellular creatures at the cell and organismal level. Damage can happen in certain locations and repair is then effected.

This of course makes evolution unlikely if there is a fundamental body plan of offspring that is generally reverted to in the face of cytoplasmic or organismal damage. To change a basic form or body plan, numerous network nodes would have to be simultaneously changed to effect the sort of necessary macro-mutations. If so, this fact would enforce the idea of immutable forms and prevent macro evolution. Hence fish would never evolve to birds, and it confirms the absurdity of expecting tigers, trees and butterflies to have a common ancestor unless miracles happen.

A blood cell (that has normally has no DNA, but had DNA artificially forced into it) won’t become a full human being if implanted in the womb, even though it has all the right DNA for the most part. Ergo, the information to code a full human must reside in the zygote cytoplasm. Granted, the cytoplasm can be reset to some undifferentiated pluripotent state in some cases, but this must be done artificially, and as far as I know, only pluripotency is achieved artificially, not totipotency.

Anyway, from Wiki:

Structural inheritance or cortical inheritance is the transmission of an epigenetic trait in a living organism by a self-perpetuating spatial structures. This is in contrast to the transmission of digital information such as is found in DNA sequences, which accounts for the vast majority of known genetic variation.

Structural inheritance has also been seen in the orientation of cilia in protozoans such as Paramecium[5] and Tetrahymena,[6] and ‘handedness’ of the spiral of the cell in Tetrahymena,[6] and shells of snails. Some organelles also have structural inheritance, such as the centriole, and the cell itself (defined by the plasma membrane) may also be an example of structural inheritance. To emphasize the difference of the molecular mechanism of structural inheritance from the canonical Watson-Crick base pairing mechanism of transmission of genetic information, the term ‘Epigenetic templating’ was introduced.[7][8]

My textbook on epigenetics at the NIH alluded to this:

A second kind of epigenetic transmission was clearly shown in Paramecia and other ciliates, in which the ciliary patterns may vary among individuals and are inherited clonally (Beisson and Sonneborn 1965). Altering the cortical pattern by microsurgery results in transmission of a new pattern to succeeding generations. It has been argued that related mechanisms are at work in metazoans, in which the organization of cellular components is influenced by localized cytoplasmic determinants in a way that can be transmitted during cell division (Grimes and Aufderheide 1991).

http://cshperspectives.cshlp.org/content/6/1/a018200.full

But really, where is structural information stored? Any takers? It seems to me the cytoplasm provides a lot of structural templating that transcends DNA as a matter of principle.

Here is a 10 minute video on structural inheritance starring creationist Arthur Jones:
http://www.metacafe.com/watch/4187488/cortical_inheritance_dna_does_not_encode_for_body_plans_dr_arthur_jones/

I think Jones is right.

Though I don’t even have a copy of Meyer’s book Darwin’s Doubt, Meyer argues:

The Sugar Code

Biologists know of an additional source of epigenetic information stored in the arrangement of sugar molecules on the exterior surface of the cell membrane. Sugars can be attached to the lipid molecules that make up the membrane itself (in which case they are called “glycolipids”), or they can be attached to the proteins embedded in the membrane (in which case they are called “glycoproteins”). Since simple sugars can be combined in many more ways than amino acids, which make up proteins, the resulting cell surface patterns can be enormously complex. As biologist Ronald Schnaar explains, “Each [sugar] building block can assume several different positions. It is as if an A could serve as four different letters, depending on whether it was standing upright, turned upside down, or laid on either of its sides. In fact, seven simple sugars can be rearranged to form hundreds of thousands of unique words, most of which have no more than five letters.”

These sequence-specific information-rich structures influence the arrangement of different cell types during embryological development. Thus, some cell biologists now refer to the arrangements of sugar molecules as the “sugar code” and compare these sequences to the digitally encoded information stored in DNA. As biochemist Hans-Joachim Gabius notes, sugars provide a system with “high-density coding” that is “essential to allow cells to communicate efficiently and swiftly through complex surface interactions.”26 According to Gabius, “These [sugar] molecules surpass amino acids and nucleotides by far in information-storing capacity.” 1 So the precisely arranged sugar molecules on the surface of cells clearly represent another source of information independent of that stored in DNA base sequences.

NEO-DARWINISM AND THE CHALLENGE OF EPIGENETIC INFORMATION

These different sources of epigenetic information in embryonic cells pose an enormous challenge to the sufficiency of the neo-Darwinian mechanism. According to neo-Darwinism, new information, form, and structure arise from natural selection acting on random mutations arising at a very low level within the biological hierarchy—within the genetic text. Yet both body-plan formation during embryological development and major morphological innovation during the history of life depend upon a specificity of arrangement at a much higher level of the organizational hierarchy, a level that DNA alone does not determine. If DNA isn’t wholly responsible for the way an embryo develops— for body-plan morphogenesis—then DNA sequences can mutate indefinitely and still not produce a new body plan, regardless of the amount of time and the number of mutational trials available to the evolutionary process. Genetic mutations are simply the wrong tool for the job at hand. Even in a best-case scenario—one that ignores the immense improbability of generating new genes by mutation and selection—mutations in DNA sequence would merely produce new genetic information. But building a new body plan requires more than just genetic information. It requires both genetic and epigenetic information—information by definition that is not stored in DNA and thus cannot be generated by mutations to the DNA. It follows that the mechanism of natural selection acting on random mutations in DNA cannot by itself generate novel body plans, such as those that first arose in the Cambrian explosion.

PS

Dr. Jones is a science and education consultant. He has a B.S. (Hons) from the University of Birmingham in biology; an M.Ed. from Bristol University and a Ph.D. in biology from the University of Birmingham. Dr. Jones has taught science and religion courses at London and Bristol Universities. He presently works for the Christian Schools’ Trust as their research consultant for curriculum development. He is a member of the Institute of Biology, London.
….
During my undergraduate days when my “heretical” views became known, my professor (Otto Lowenstein, Professor of Zoology) made a point of telling me that no creationist would be allowed to do research in his department! However, he did allow me to do research. From the pressure that was put on me, I can only assume that it was thought that I could be convinced of the error of my ways. If that was the intention, then it badly backfired. Many a visiting scholar was brought into my laboratory to convince me, from their area of expertise, that evolution was indisputably true. Of course, hardly knowing their field, I never had an answer at the time, but after they had gone I would look up the relevant research and carefully analyze it. I always found that the evolutionist case was much weaker than it had seemed and that alternative creationist interpretations were available which were just as or more convincing. My position was further strengthened by the results of my own research.
https://answersingenesis.org/creation-scientists/arthur-jones-biology/

63 thoughts on “Non-DNA Structural Inheritance

  1. I have a suggestion for you, Sal. Copy this post to the professors in your molecular biology class and ask them if they agree with you. Since they’re well-respected, grant-rich Nobelists and always right, you should value their opinions.

  2. Sal,
    This is a very interesting topic and well worth a lengthy discussion!!

    I think you have generally the right idea on this. I have the impression that you go wrong when you rigidly adhere to certain definitions and concepts.
    My take on it is this: there is certainly information contained in the cell outside the nucleus. But this information is not of the same sort you’d find in DNA. Its the sort you’d find in any 3-D object. I’m not sure how you’d define these different types of information; whether you’d call the DNA first order information and the cell structure 2nd or 3rd order, or whether you’d define it in terms of a chain of cause-and-effect. I dont know how to define it but I know theres a difference.
    If this seems like a problem for our understanding of cell structure or inheritance I think thats because one has a misconception about what DNA is doing. DNA doesnt code for how to ‘make’ a cell. It codes for how to maintain a cell. If one asks where that cell came from in the first place the answer is that the cell with its DNA has been evolving for billions of years.

  3. Sal,
    This is a very interesting topic and well worth a lengthy discussion!!

    I think you have generally the right idea on this.

    Thanks.

    I have the impression that you go wrong when you rigidly adhere to certain definitions and concepts.

    Suggestions to improve my understanding are always welcome.

    Imho, we humans out of necessity try to explain things in the most simple terms. Mutate a single nucleotide in the right location and the organism is radically changed, hence we are tempted to think DNA controls everything.

    Damage a piece of the cytoplasm, and nothing long term seems to happen, therefore we think the cytoplasm can’t be information bearing. I

    Systems capable of self-healing through a network topology will give the illusion the components of the system are dispensable and hence not information bearing — certainly not for heritable features.

    The line of argument I has posed is that if DNA only codes for proteins and helps regulate protein quantities, that is only a necessary but not sufficient condition for implementing a body plan. The central dogma could be true as far as DNA-to-protein coding, but part of the body plan information could still be outside the domain of the central dogma.

    The prion is one example of structural inheritance that transcends the central dogma (which I’m mostly OK with), so this suggest other structural information can exist outside the DNA, and it would seem must exist outside DNA if DNA only holds the protein sequences and some expression level data.

    Prion:

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

    A prion (Listeni/ˈpriːɒn/[1]) is an infectious agent thought to be the cause of the transmissible spongiform encephalopathies (TSEs). It is composed entirely of protein material, called PrP (short for prion protein), that can fold in multiple, structurally distinct ways, at least one of which is transmissible to other prion proteins, leading to disease that is similar to viral infection. The word prion, coined in 1982 by Stanley B. Prusiner, is a portmanteau derived from protein and infection, hence prion, and is short for “proteinaceous infectious particle”,[2] in reference to its ability to self-propagate and transmit its conformation to other proteins.[3]

    I think structural heredity on organismal scales is far more complex than the prion example, but the prion example is a small starting point for seeing there a possibility of non-DNA structural inheritance.

    I’m sympathetic to the glycome as a huge repository for such information, but sequencing the glycome is brutally difficult and not feasible on large scale as we are able to do with DNA. I don’t think we’re anywhere close to answering the question of where and how body plan or cell structure information is stored and duplicated.

  4. Mutate a single nucleotide in the right location and the organism is radically changed, hence we are tempted to think DNA controls everything.

    It does for the most part, either directly or indirectly, but mutating that vast majority of nucleotides would have no effect at all. .

    Damage a piece of the cytoplasm, and nothing long term seems to happen

    There are many places where it would have profound effect. Look up early development in the fruitfly. There are mRNAs that are injected into the egg from the mothers cells that direct anterior-posterior patterning. They localize to only one part of the egg where they determine the head or posterior. They localize there because they stick to proteins which stick to other proteins which stick to parts of the cytoskeleton. The A-P axis of the cytoskeleton comes from the mothers cells that form the egg. So the orientation of the A-P is passed down from generation to generation.

    The line of argument I has posed is that if DNA only codes for proteins and helps regulate protein quantities

    DNA does much more than that, in part because proteins themselves contain information. Consider 2 proteins, A and B. Both are enzymes that catalyze the same reaction at the same rate and both are 300 amino acids long. Protein A floats in the cytoplasm. Protein B is localized to a particular place in the cell because of its ability to bind cytoskeletal components. It also self-assembles with other enzymes to make an efficient multi-protein complex and it binds to its product and as a result has negative-feedback inhibition. Wouldnt we say that the DNA sequence that codes for B has more information than the sequence that codes for A? **

    The prion is one example of structural inheritance that transcends the central dogma

    According to the original definition of the Central Dogma prions are not in violation of it. The information they pass on is rather trivial -and it isn’t coded.

    **( 15 years ago I had the notion of writing a book on the many layers of information in the genome and the cell. But I can barely write blog comments much less books)

  5. Thanks for your helpful comments. I’m inclined now to take some developmental biology classes in light of your comments.

    One part of the proteome which appears not to have direct DNA influence are the large suite of post translational modifications. Histone modifications are a well-known set of post translational modifications, but there are way more than just histone proteins being modified, and these modifications don’t have a simple mapping from DNA like the codon table to amino acids.

    We sort of know the machinery proximally, but the long chain of events and components leading to the post translational modifications are so deep that no one is able to trace from start to finish.

    Lots of proteins have disulfide bonds. Where is the simple mapping from DNA to the protein that says “put a disulfide bond here”. It’s not in the condon table.

    We sort of know some of the proteins that effect some post translational modifications, but then some of these complexes are very intricate and some involve non-coding RNAs and who knows what else.

    Our experimental techniques to elucidate these interactions though advanced in many respects are also crude. We must surely be missing a lot of pieces when we hack the cell apart and look at which parts are still sticking together to make a guess at what is really going on.

    There are mRNAs that are injected into the egg from the mothers cells that direct anterior-posterior patterning. They localize to only one part of the egg where they determine the head or posterior. They localize there because they stick to proteins which stick to other proteins which stick to parts of the cytoskeleton. The A-P axis of the cytoskeleton comes from the mothers cells that form the egg. So the orientation of the A-P is passed down from generation to generation.

    Amazing. Thanks.

    Perhaps of some interest:

    Majority of eukaryotic proteins are glycosylated and their glycan moieties have numerous important structural, functional and regulatory roles. Because of structural complexity of glycans and technological limitations glycomics, and particularly glycoproteomics was not able to follow rapid progress in genomics and proteomics over last 30 years. However, the field of glycan has been progressing rapidly and first large-scale studies of the glycome have been completed recently. These studies have revealed significant differences in glycome composition between individuals, which may contribute to the human phenotypic variability. The current state-of-the-art in high-throughput glycomics and its integration with genomics, epigenomics and lipidomics is reviewed in this article.

    http://www.sciencedirect.com.mutex.gmu.edu/science/article/pii/S1367593112001573

  6. where is the developmental or structural information? I’ve never gotten a straight answer from most evolutionists I’ve encountered

    You’d be asking the wrong people then. I don’t know why you’d think evolutionists would have a very strong grasp of the details of phenotypic expression. Phenotype is something of a ‘black box’ to the evolutionist – it’s not vitally important to an understanding of evolution, which is why the same equations broadly apply to any sexual species: fungus, plant, animal or protist (there are equations that apply to asexuals too, but much of classical pop-gen assumes panmictic populations of sexuals).

    Selection acts via phenotype to sort allele frequencies (genotype, typically, though other forms of ‘allele’ may be envisaged). How phenotype is extracted does not much matter. But there seems little doubt that developmental and structural elements are genetically encoded. Hence consistency of form and behaviour over the long term, via both sperm and egg.

  7. It would seem, if DNA is mostly about storing the data for protein sequences, as a matter of principle it doesn’t store the structural information for cells and entire bodies. The information is elsewhere, likely in the cytoplasm of the zygote.

    How does it get there and how is it implemented? Where does cytoplasm come from?

  8. stcorva: It would seem, if DNA is mostly about storing the data for protein sequences, as a matter of principle it doesn’t store the structural information for cells and entire bodies.

    As a matter of principle? WTF?

  9. Strange, if DNA does not store the information for development, how developmental mutants are genetic mutants. Of course one can screw with expression, and imagine one is doing something ‘epigenetic’. But I’m betting DNA is seen as central for a reason. People did not just make this up.

  10. stcordova,

    The central dogma could be true as far as DNA-to-protein coding, but part of the body plan information could still be outside the domain of the central dogma.

    Find it, and grab yourself a Nobel.

    Transcription factors are transcribed too. Binding sites occupy real bits of DNA. Methylatable regions too occupy DNA bits. So do the enzymes that write and wipe. So do the factors influenced by developmental hormones. And so on.

  11. stcordova: Lots of proteins have disulfide bonds. Where is the simple mapping from DNA to the protein that says “put a disulfide bond here”. It’s not in the condon table.

    Could it conceivably have something to do with a cysteine and another cysteine? Just spitballing here.

  12. stcordova,

    One part of the proteome which appears not to have direct DNA influence are the large suite of post translational modifications.

    Wha? How ‘direct’ does it have to be for DNA to be causal? What performs post translational modification, if not coded enzymes? Anything can be a substrate for an enzyme, including DNA, RNA and protein.

  13. Allan:

    Wha? How ‘direct’ does it have to be for DNA to be causal? What performs post translational modification, if not coded enzymes? Anything can be a substrate for an enzyme, including DNA, RNA and protein.

    Thanks anyway for the conversation, but the fact that DNA is necessarily causal, doesn’t imply that DNA is sufficiently causal. That is basic logic.

    Just because DNA codes for the parts does not at all imply it contains information for how the parts are to assemble and operate.

    Strange, if DNA does not store the information for development, how developmental mutants are genetic mutants.

    That would be still true if DNA is causally necessary, but not causally sufficient. The facts you state about genetic mutation destroying developmental mutation establishes only DNA necessity, not sufficiency.

    Just as a review of basic logic:
    http://www.txstate.edu/philosophy/resources/fallacy-definitions/Confusion-of-Necessary.html

    Confusion of Necessary with a Sufficient Condition

    you commit this fallacy when you assume that a necessary condition of an event is sufficient for the event to occur. A necessary condition is a condition that must be present for an event to occur. A sufficient condition is a condition or set of conditions that will produce the event. A necessary condition must be there, but it alone does not provide sufficient cause for the occurrence of the event. Only the sufficient grounds can do this. In other words, all of the necessary elements must be there.

    Examples:
    1.Juan: “How do you think you’ll do on our philosophy exam tomorrow?” Monique: “Great, I read all the books.” Juan: “Yeah but do you understand this stuff?” Monique: “I said I read all the books, didn’t I?”
    2.Don’t let all the talk about the necessity of exercise to a long life mislead you. Jim was a jock all his very short life.
    3.Who said food keeps us alive? Tom died a few days ago and he was not short of good food.
    4.I don’t know why the car won’t run; I just filled the gas tank.
    5.Why don’t you want to spend your life with me? I love you, and am I not good to you?
    6.The counselor told me that if I wanted to graduate I must have at least 128 credit hours. Well, I’ve got that, but they’re saying I won’t walk this semester. How misleading!
    7.The job description said that they were looking for someone with a Master’s degree. I’ve got my MA, but I cannot understand why they did not hire me.
    8.My high school English teacher told me successful people have extensive vocabularies. So, I’ve tried to learn a new vocabulary word every day since then. I should be a successful person soon.
    9.”If you want the chairman to like you,” he said, “you’ll have to show how impressed you are with his ideas.” Well, I turned myself into an ego-stroking machine, but it’s pretty clear I have yet to win him over.
    10.I’ve heard this ever since puberty: in order to fall in love with another, you have first to love yourself. This is such a crock! I have no trouble loving myself, bit I can’t say I’ve ever fallen in love in my life.

    The claim “DNA is causally necessary therefore DNA causally is sufficient” is a fallacy like those quoted above.

    Of course one can screw with expression, and imagine one is doing something ‘epigenetic’. But I’m betting DNA is seen as central for a reason. People did not just make this up.

    The issues is not that DNA is necessary, the issue is whether DNA is sufficient. It is not. Put DNA in the wrong cytoplasmic context and it does nothing.

    A living creature is a sufficient condition to be a living creature, DNA is not a sufficient condition.

    Cytoplasm alone is almost but not quite a sufficient condition as evidenced by the fact enucleated cells that duplicate up to the blastula stage. Enucleated cells can “live” for a while (as in metabolize). In contrast, DNA by itself won’t even get that far.

    So, I think what is sufficiently causal is a complete living system or population (male and female or whatever), not a partial system like DNA in isolation.

  14. Morphology and structure is emergent. The constituents are produced in certain quantities and at certain times (themselves dependent on context, environment, cytoplasmic constituents and DNA sequence), and the resulting structures are emergent from the interactions between all these things.

    This information doesn’t exist anywhere in the normal sense we use to say for example protein sequence exists in DNA. You will never be able to read a DNA sequence and then predict, without some a priori knowledge of environmental circumstances, genes already expressed and so on, what structure will result therefrom.

    In fact you can’t even say the structure exists “as information” before it comes to be, when it is the result of interactions rather than some sort of digital or analogous coding principle. The structures come to exist due to the properties of the molecules and their interactions. It is neither in the DNA nor the cytoplasm or even in the external environment. It is due to all three things interacting, but it is not “encoded/stored there” in any way I understand the term “information” and “encoded/stored” to mean.
    To say that it is “encoded” in the DNA (or that it “exists in the cytoplasm or w/e”) can’t be more than a metaphor in that sense.

    What might produce a beatiful icosahedron viral capsid at 37 degrees C will produce a misfolding piece of junk at 121 degrees C. That’s because the “context”, the environment wherein the proteins fold and interact has changed. You can’t pick any single thing out and say “that’s where the information for the structure is” without including all the other internal and external factors.

  15. Here is a popular description of glycans that alludes to why Gene-centrism is the wrong way to perceive biology. I’ve advocated Whole-centrism. But anyway:

    http://phys.org/news/2012-06-tools-unveil-mystery-glycome.html

    New tools developed to unveil mystery of the ‘glycome’

    The “glycome”—the full set of sugar molecules in living things and even viruses—has been one of the least understood domains of biology. While the glycome encodes key information that regulates things such as cell trafficking events and cell signaling, this information has been relatively difficult to “decode.” Unlike proteins, which are relatively straightforward translations of genetic information, functional sugars have no clear counterparts or “templates” in the genome.

    The important development is they are finding ways to “mutate” the glycome independent of the genome. Speculative prediction: such technology advances will highlight features of glycome that DNA is necessary but not sufficient to create.

    If there is no direct way DNA can some but not ALL aspects of the glycome, but the glycome can be modified by environmental factors or other non-DNA factors, and if the glycome is important to structural inheritance, then this implies there is non-DNA structural inheritance.

    However, if there is a self-healing network topology for storing the information in the glycome, then damage to the glycome can be prevented from appearing in subsequent generations of the cell or species line.

    If for example, 90% of the copies of book were destroyed, or if we were only left with fragments, if we have enough fragments, we can reconstruct the information. That is an example of a distributed information storage network that is at least capable of self-healing in principle.

    The information in DNA is localizable to one physical location. In contrast, the information of the glycome, like a book with many copies and fragments, is likely distributed and redundantly stored in the cell. If there were not redundancy in the cell, injuries to the cytoplasm would not be repairable.

    The experiment showed how at least one small set of all glycans can be affected in a cell resulting in a complete shutdown.

  16. Sal
    I think Rumraket has it right.
    The information in the DNA only functions within the context of an environment. That environment can include 3dimensional structures which serve as a scaffold or template for modification. Of course the components of the scaffold are coded for in the DNA, along with the timing of their production and localization but there is no time in the life of the cell or species when the scaffold is not there and it cannot be created from scratch. There are many parts of the cell that have this property.
    There are also cases where complexity can be generated from the information in the DNA and a template is not needed. This is true for the most part in the case of animal body plans. The only 3d information present in the zygote may be the body axes but this is rather trival. Most of the complexity of the body is generated entirely from instructions in the DNA

  17. Although I think this is a very interesting discussion lets not forget that the ultimate purpose of the arguments you and Arthur Jones are making is to somehow undermine evolution.
    I think Jones’ strategy is to discredit biologists in the eyes of his followers- if biologists don’t really know whats going on with genes how can they know anything about evolution?. The thing is that even if Jones is correct in everything he says this is no more a problem for evolution than it is for special creation. And most of the evidence for evolution are irrelevant to this issue.
    I think Jones’ claims are so off they verge on dishonesty

  18. One can choose whichever stance one finds most informative. But the idea ‘gene centrism is the wrong way’ because there are things in cytoplasm is just bollocks.

    I think it has more to do with the fact that Dawkins champions this view, and we don’t want any credence to go the way of atheist scum, do we kids?

  19. stcordova,

    Cytoplasm alone is almost but not quite a sufficient condition as evidenced by the fact enucleated cells that duplicate up to the blastula stage.

    That proves nothing more than that DNA does not need to be read continuously. You can take death cap and will feel fine for 20 hours or so. Until the lack of translation starts to become a bit of an issue.

  20. stcordova,

    Just as a review of basic logic:[…]

    Spare me the patronisation. Everything in the cytoplasm is manufactured via a DNA template. All of it. Including, of course, the things that read the template.

  21. Why does posttranslational modification occupy a position in this argument that (say) lactate dehydrogenase does not?

  22. Allan Miller: I think it has more to do with the fact that Dawkins champions this view, and we don’t want any credence to go the way of atheist scum, do we kids?

    Those WEASELs!

  23. Allan Miller: Everything in the cytoplasm is manufactured via a DNA template. All of it. Including, of course, the things that read the template.

    Do you think software developers are nothing more than template makers?

    The Excel executable is just a template for making spreadsheets!

  24. I think Sal is pulling a fast one here. Consider a hypothetical system where a nucleic acid is a ‘true’ self-replicator. It can generate template copies of itself. Now, a modification asists it in doing the job better via production of a small molecule from part of the DNA template. Eventually, replication becomes so tuned to the presence of this molecule that it cannot proceed successfully without it.

    Then, someone pulls a fast one with some guff about necessity, sufficiency and gene-centrism, because ‘DNA alone’ cannot replicate. Basically, all phenotype is (in Sal’s view) fatal to gene centrism. Which is wrong.

  25. Mung,

    Do you think software developers are nothing more than template makers?

    The Excel executable is just a template for making spreadsheets!

    I think software analogies have considerable power to mislead.

  26. Spare me the patronisation. Everything in the cytoplasm is manufactured via a DNA template. All of it. Including, of course, the things that read the template.

    1. your logic is still flawed, if you take offense sorry, but it’s still flawed, I described why your viewpoint is flawed in painful detail. Sorry if you viewed it as patronizing, but well, I was also defending my position and so I laid out my case why I think your view is wrong.

    2. the DNA template specifying the sequence doesn’t specify the connections and assembly and all the operational details

    3. your assertion is wrong that DNA is a template for everything in the cytoplasm, not the least of which are the exact sequences and chemical states of the glycans, the glycoproteins complexes, the glycolipid complexes, etc. I provided some of the cutting edge chemical experiments. Where is there a DNA template for the glycans?

    4. there are 100 trillion cells in the adult human, many are radically different than other cells. They mostly have the same DNA, but what makes the cells duplicate differently? The cytoplasm. For that matter, without a mother, that poor little zygote doesn’t have much of chance. You have an awfully simplistic view of how information is conveyed from one generation to the next.

  27. A criminologist complains about how epigenetics is used in his field:
    Epigenetics Has Become Dangerously Fashionable

    It is important to point out that non-DNA inheritance does not imply that acquired characteristics are easily passed on to the next generation. For example, an amputee can have normal children because the cytoplasm of the sperm or egg are not affected to such a severe degree by the amputation that the next generation acquires the anatomy of the parent with the amputation.

    I’m not saying that epigenetic inheritance implies large scale heritable epigenetic changes but rather persistent epigenetic developmental information.

    The OP is focusing on more specific chemical mechanism that stores information for the construction of organs and limbs. No one has made a convincing argument that all of that information resides solely in the DNA.

    I’ve provided some data that suggest the information repository for formation of organs and limbs is not solely in the DNA. A heart “cell” has the same DNA as a zygote — it doesn’t imply they will generate the same physical structures. So something is different in those cells other than DNA. What is it? No one knows exactly, but it clearly isn’t the DNA since the DNA is mostly identical between those cells.

  28. A lethal epigenetic cocktail

    November 26, 2012

    There are two deeply disturbing properties of epigenetic inheritance that have been receiving much attention of late. The first is the ability of certain classes of chemicals to cause epigenetic changes that can be transmitted transgenerationally. The second is the propensity of genetically stable tumor cells to display great epigenetic variation, driving their evolution and malignancy.

    Manikkam et al [PLOS ONE 7(9):e46249] report that Dioxin, a potent epimutagen, can induce multiple adult onset disease in the F3 generation when administered to gestating female rats. In another important study Ujvari and coworkers (Proc Biol Sci. 2012 Nov 7. [Epub ahead of print]) find that a bizarre transmissable facial cancer in the Tasmanian Devil, although genomically stable, undergoes extensive epigenetic changes that drive its tumorigenicity. Because of this variability the tumors evolves over time, and these changes can be transmitted to other animals through bodily contact. This rare marsupial has been pushed to the edge of extinction by this cancer.
    – See more at: http://www.newportbiotech.com/pages/blog/entry/10/#sthash.4i6s8PAl.dpuf

    Research into epigenetics is not a passing fad, it is driven by researchers of cancer and other medical issues. Chemical modifications of non-DNA components of biological systems can occasionally result in damaging short or long term heritable changes.

    But again, most of the epigenetics I point out in the OP is not focused on acquired characteristics but rather persistent epigenetic features. Here is a persistent epigenetic mark that occurs over and over again on the female X-chromosome:

    https://en.wikipedia.org/wiki/X-inactivation

    X-inactivation (also called lyonization) is a process by which one of the copies of the X chromosome present in female mammals is inactivated. The inactive X chromosome is silenced by its being packaged in such a way that it has a transcriptionally inactive structure called heterochromatin. As nearly all female mammals have two X chromosomes, X-inactivation prevents them from having twice as many X chromosome gene products as males, who only possess a single copy of the X chromosome (see dosage compensation). The choice of which X chromosome will be inactivated is random in placental mammals such as humans, but once an X chromosome is inactivated it will remain inactive throughout the lifetime of the cell and its descendants in the organism. Unlike the random X-inactivation in placental mammals, inactivation in marsupials applies exclusively to the paternally derived X chromosome.

    ….
    ; X-inactivation, which is an epigenetic change that results in a different phenotype, is not a change at the genotypic level.

  29. stcordova: You have an awfully simplistic view of how information is conveyed from one generation to the next.

    I can’t wait to read your paper enlightening us all.

  30. OMagain: I can’t wait to read your paper enlightening us all.

    I’m waiting patiently for how it’s done.

    A theory that accounts for all the evidence.

    While he’s at it, perhaps Sal will talk to us about how royal jelly works.

  31. I asserted in the OP that developmental information is redundantly stored in biological systems, parts of the developmental information can be knocked out and the target organ or structure will still form correctly via another developmental mechanism. Here is evidence to that effect. I discussed it at UD 10 years ago, and although mathematician Jason Rosenhouse and developmental biologist Richard Aczevedo disputed it, they didn’t refute it:

    http://www.uncommondescent.com/intelligent-design/airplane-magnetos-contingency-designs-and-reasons-id-will-prevail/

    I quoted Denton:

    The phenomenon of redundant genes is so widespread that it is already acknowledge to pose something of an evolutionary conundrum. Although in the words of the author of one recent article, “true genetic redundancy ought to be, in an evolutionary sense, impossible or at least unlikely,” partially redundant genes are common. As another authority comments in recent review article: “Arguments over whether there can be true redundancy are moot for the experimentalist. The question is how the functions for partially redundant genes can be discovered given that partial redundancy is the rule.

    And it seems increasingly that it is not only individual genes that are redundant, but rather that the phenomenon may be all-pervasive in the development of higher organisms, existing at every level from individual genes to the most complex developmental processes. For example, individual nerve axons, like guided missiles or migrating birds, are guided to their targets by a number of different and individually redundant mechanisms and clues. The development of the female sexual organ, the vulva, in the nematode provides perhaps the most dramatic example to date of redundancy exploited as a fail-safe device at the very highest level. A detailed description of the mechanism of formation of the nematode vulva is beyond the scope of this chapter, suffice it to say that the organ is generated by means of two quite different developmental mechanism, either of which is sufficient by itself to generate a perfect vulva.

    It seems increasingly likely that redundancy will prove to be universally exploited in many key aspects of the development of higher organisms, for precisely the same reason it is utilized in many other areas–as a fail safe mechanism to ensure that developmental goals are achieved with what amounts to a virtually zero error rate.

    Now, this phenomenon poses an additional challenge to the idea that organisms can be radically transformed as a result of a succession of small independent changes, as Darwinian theory supposes. For it means that if an advantageous change is to occur, in an organ system such as the nematode vulva, which is specified in two completely different ways, then this will of necessity require simultaneous changes in both blueprints. In other words, the greater the degree of redundancy, the greater the need for simultaneous mutation to effect evolutionary change and the more difficult it is to believe that evolutionary change could have been engineered without intelligent direction.

    But in any case here is the paper and the relevant section:

    A perfect Vulva Every Time
    Together these recent papers provide very strong evidence that both a graded morphogen and a sequential signaling cascade can act to pattern a single set of cells during development. They do not indicate which of the twosignaling mechanisms plays the predominant role during normal development. However, a simple and attractive model is that the two pathways both operate and are partially or fully redundant. This set-up would enable the vulva
    to form perfectly in every animal, which it does.

    ….
    In summary, the great debate between the champions of gradients and cascades may end in a draw. In C. elegans, it looks as though the pattern of vulval cell fates can be specified in either way: by using a single graded signal
    that emanates from a central source or by using a relay system in which one signaling cell tells its neighbors to produce a second signal, which, in turn, patterns more remote cells. When either system is eliminated, all the
    vulval cell fates can still be produced. If these two systems both operate during normal development, then together they could produce the ever-perfect tiny vulvae that C. elegans is so famous for.

    If the information in the glycans is redundantly distributed in a way that allows self-healing and very very deep redundancy, then unlike DNA, which can be mutated by mutating a single nucleotide at a time, deeply redundant glycan or other cytoplasmic information cannot be mutated by mutating a single location at a time, but requires mutation in several locations to effect a heritable change.

    BITCOIN and other information network architectures in the man-made world illustrate that the larger the network distribution of information and the deeper the redundancy, the greater the difficulty of “mutating” mission critical information with errors.

    Because a variety of injuries to the cytoplasm seems shrugged off by a cell, and that duplication and development proceeds normally, it is easy to assume there is no developmental information in the injured parts, but this is an errant view.

    For example, if someone gets at small scrape or cut on their hand, they heal easily. It is easy to presume the skin cells that got scraped off or injured weren’t information bearing. This naïve view is easily falsified by observing when more and more skin is removed due to injury, there comes a point healing is compromised. Hence this illustrates distributed network topology for developmental information.

    What is witnessed at the organismal level is witnessed at the cellular level as well.

  32. stcordova: A heart “cell” has the same DNA as a zygote — it doesn’t imply they will generate the same physical structures. So something is different in those cells other than DNA. What is it?

    Their location in the body and the surroundings of the individual cells. The cell responds to it’s environment with a different expression pattern. It is entirely possible to explain all their differences in terms of their surroundings causing different gene expression patterns.

    stcordova: 4. there are 100 trillion cells in the adult human, many are radically different than other cells. They mostly have the same DNA, but what makes the cells duplicate differently? The cytoplasm.

    What’s in the cytoplasm? Molecules produced by genes expressed in the nucleus. Expressed due to the environmental stimuli that caused those expression patterns.

    stcordova: If there were not redundancy in the cell, injuries to the cytoplasm would not be repairable.

    What the hell does “injury to the cytoplasm” even mean? Are you talking about mere changes in the concentrations of the compounds that exist therein? In the classic Lac Operon example, as cytoplasmic glucose concentration drops the gene for beta-galactosidase expression activates. If later on the cell again encounters glucose, it will inhibit beta-galactosidase expression and the cell will start metabolizing glucose instead. There is nothing in the cytoplasm that is not, at least in principle, restorable by changing expression patterns around.

    stcordova: No one has made a convincing argument that all of that information resides solely in the DNA.

    That’s because nobody actually believes it does. Rather the resulting morphological structures are emergent properties of all the interacting parts. Change the enviroment enough and the same genetic program will produce a different result despite no actual nucleotide changes, because the environment will have affected how the gene-products interact with each other. I’ve already given a simple concrete example with the icosahedral viral capsid.

    stcordova: 2. the DNA template specifying the sequence doesn’t specify the connections and assembly and all the operational details

    Neither does any particular thing in the cytoplams, nor even “all of the cytoplasm”. None of these things can be looked at in isolation and be said to be where “it’s all stored”.

    stcordova: Cytoplasm alone is almost but not quite a sufficient condition as evidenced by the fact enucleated cells that duplicate up to the blastula stage. Enucleated cells can “live” for a while (as in metabolize). In contrast, DNA by itself won’t even get that far.

    There is no such thing as “cytoplasm alone”. The cytoplasm is the contents of the cell, excluding the nucleus and several large organelles. To have “cytoplasm” you need a membrane around it. To have a membrane you need phospholipids, to have phospholipids you need enzymes to produce them. To have enzymes you need translation, to have something to translate you need transcription, to have transcription you need a genome. The membrane is chock full of transport proteins, all of them produced by genes that are transcribed and translated.

    The reason an enucleated cell can live on for a while is because it already contains all the things that were previously produced by that nucleus and the translation system. Countless types of membrane transport proteins, mature mRNA which can be continously translated until it breaks down, enzymes that produce all these things and so on and so forth. Where did all these things come from? A nucleated cell. You’re coming along after the fact, after the nucleus has done much of it’s job producing countless gene products required for cell-division, then removing the nucleus and saying “oh look, it keeps going even without a nucleus, at least for a while“. Why would you have expected differently? What does that prove? Nothing, it is as much an argument for the indispensibility of the nucleus as it is against it.

  33. It is entirely possible to explain all their differences in terms of their surroundings causing different gene expression patterns.

    You used the word “all” the available data suggest “some” or “most” but certainly not “all”.

    Change the enviroment enough and the same genetic program will produce a different result despite no actual nucleotide changes, because the environment will have affected how the gene-products interact with each other. I’ve already given a simple concrete example with the icosahedral viral capsid.

    You assume the program is purely genetic, and it is not. Showing some change with a simple example does not imply all change.

    gene-products interact with each other.

    You call them “gene-products” but they are products of more than genes. Genes by themselves don’t make anything without the machinery. This is like saying the “product of blue prints” when “product of factory” is more accurate.

    I’ve already pointed out glycan structure isn’t dictated in by a simple DNA template. One might say, “this DNA codes for this protein or ncRNA”, one can’t say however “this DNA codes for this glycan or glycoprotein or glycolipd”. Just because DNA may code for the necessary proteins that are used to make the glycans does not imply that DNA provides the sufficient technology to coordinate the proteins to make glycans.

    It is a basic logic error to confuse necessary with sufficient conditions. DNA is necessary, it most certainly is not sufficient.

    A protein’s function is more than the sequence of amino acids, but how it is folded. There are many possible folds and for a system or workable interacting folds, only a small space of a set of folds will lead to a working system. This leads to the levinthal paradox of the protein interactome.

    http://www.ncbi.nlm.nih.gov/pubmed/21987416
    The Levinthal paradox of the interactome

    The central biological question of the 21st century is: how does a viable cell emerge from the bewildering combinatorial complexity of its molecular components? Here, we estimate the combinatorics of self-assembling the protein constituents of a yeast cell, a number so vast that the functional interactome could only have emerged by iterative hierarchic assembly of its component sub-assemblies. A protein can undergo both reversible denaturation and hierarchic self-assembly spontaneously, but a functioning interactome must expend energy to achieve viability. Consequently, it is implausible that a completely “denatured” cell could be reversibly renatured spontaneously, like a protein. Instead, new cells are generated by the division of pre-existing cells, an unbroken chain of renewal tracking back through contingent conditions and evolving responses to the origin of life on the prebiotic earth. We surmise that this non-deterministic temporal continuum could not be reconstructed de novo under present conditions.
    ….
    Assuming the simplest case that each of n proteins is present in a single copy in the proteome and all proteins engage in pairwise interactions (Fig. 1), the total number of possible distinct patterns of interactions is:
    (for details of calculations, cf. Supporting Information). For n = 4500, this is on the order of 10^7200, an unimaginably large number; but a more realistic calculation is yet more complicated. With an average of 3540 distinct interfaces for a single protein, there are 4500 × 3540 = 1.6 × 10^7 entities, resulting in 10^(5.4×10^7) possible distinct interaction patterns (cf. Supporting Information). If proteins are present in 3000 copies instead of a single copy, identical pairwise complexes of the same pair should not add to multiplicity of interactions patterns; nevertheless, the number of distinct interactomes increases further because different copies of the same protein can engage in interactions with different partners at the same time. In this case, the estimated number of different interactomes is on the order of 10^(7.9×10^10) (cf. Supporting Information).

    Put a frog in a blender and one will have all the “gene products”, but all those “gene products” does not a frog make. The above paper shows how naïve it is to suppose DNA and gene expression solely defines heritable features. It does not. Kill the interactome, the cytoplasm, there isn’t any inheritance to speak of because the cell will be dead.

  34. stcordova: The above paper shows how naïve it is to suppose DNA and gene expression solely defines heritable features.

    Sal,
    I think you’ve missed the point of the above paper. It has nothing to do with whether DNA determines heritable features- DNA does determine the vast majority of them though.
    I think its addressing the claims of people like Craig Venter who think they’ll one day be able to assemble a new form of life – a new cell- from scratch.
    If you read the last few sentences you’ll see they’re saying pretty much the same things Rumraket and I have been saying

  35. stcordova: Put a frog in a blender and one will have all the “gene products”, but all those “gene products” does not a frog make. The above paper shows how naïve it is to suppose DNA and gene expression solely defines heritable features. It does not. Kill the interactome, the cytoplasm, there isn’t any inheritance to speak of because the cell will be dead.

    Good job of trying hard not to understand there Sal.

  36. Another cue to bad science: the coinage of a new term ending in “-ome”. Not perfect — after all, “genome” is such a coinage” — but a good rule of thumb. Sal’s posts have a sizable bullshitome.

  37. John Harshman:
    Another cue to bad science: the coinage of a new term ending in “-ome”. Not perfect — after all, “genome” is such a coinage” — but a good rule of thumb. Sal’s posts have a sizable bullshitome.

    But do they have information?

  38. Good grief. Been away for a few days, it’s the ‘frog-in-a-blender proves DNA is not central’ argument. Stick me naked on a hillside in Iceland and it’ll prove that I’m nothing without my coat. Which, not entirely coincidentally, is where I’m off shortly, so maybe I’ll give it a whirl.

    The point Sal et al (and Lizzie’s admired Denis Noble) miss is that gene-centrism is not a developmental stance anyway, but an evolutionary one. I’ll just say that, without further elaboration, ‘cos it’s pointless talking to someone whose fingers are jabbed firmly in their ears.

  39. I wrote a post yesterday but when I pressed post there was some database issue. Luckily I had it saved but now I can’t find the damn text file xD

  40. Alan Fox:

    John Harshman: Another cue to bad science: the coinage of a new term ending in “-ome”.

    Is that a new phenomenome?

    Relatively. But after Seymour Benzer’s 1961 coinage of the words “cistron”, “recon” and “muton”, there was a period of bad “-on” words.

  41. stcordova: You assume the program is purely genetic, and it is not.

    But I’m not saying that, Sal. In some respects I’m actually agreeing with you. Body-plans are not encoded in the genome alone.

    But it’s also not “in the cytoplasm”.

    What I’m saying is body plans aren’t encoded at all, that they cannot be reduced to any particular thing. Whether that be cytoplasm, nucleotide sequences or protein folding. Body plans are an emergent property of ALL of it. They don’t have “representations” anywhere in the same way that amino acid-sequence has a “representation” in RNA and DNA sequence.

    The point of the icosahedron that make up many viral capsids, as an example of what I mean, is that it is simple to show how all the different factors end up affecting the capsid structure. “Ideally” the capsid proteins are produced, then they fold correctly into the different polygon “faces” of the icosahedron once they emerge from the ribosome. Then in the cytoplasm, they interact and assemble into the capsid icosahedron. But the external environment of the cell affects the folding of the proteins and their interactions in the cytoplasm. If it is too hot, or too salty, either there will me mistranslation, or misfolding, so the shape of the folded protein will change, possibly even denature, which will cause it to change the shape of the capsid, or even prevent them from sticking together and form the capsid. Notice how nothing can be ignored here to explain how the icosahedron takes shape. You need the genome to explain the amino acid sequence of the protein. You need the temperature and salt concentrations to explain protein folding and their interactions.

    Where is the icosahedron “encoded” then? Nowhere in particular. It emerges once a whole host of conditions are satisfied, change the conditions and you change the icosahedron. Temperature alone will do that. Keep the cytoplasm and genome constant, just bump the temperature to 121 degrees C and the protein will misfold = no icosahedron. Change the nucleotide sequence so the amino acid sequence is changed in key locations = no icosahedron. Add lots of ammoniumsulfate to the cytoplasm = proteins misfold and aggregate = no icosahedron.

    They all have to work together. No one thing is the cause of structures. No one thing can be looked at in isolation and the resulting morphological structures predicted therefrom. Gene-centrism is nor more wrong than cytoplasm-centrism in explaining morphology.

  42. Rumraket: Gene-centrism is nor more wrong than cytoplasm-centrism in explaining morphology.

    I would put it somewhat differently. I would say that genomes are automata in the sense used by Wolfram. They unfold or evolve, and the outcome is dependent on the attributes of the playing field as they unfold. The unfolding also modifies the playing field.

    One of the interesting characteristics of Wolfram automata is that it can be impossible to tell what will be produced from a given starting configuration.

  43. DNA, the physical substance, is actually as much phenotype as genotype. More so, in many respects. Gene-centrism relates to the passage of sequential information down the generations and across populations, not to any particular physical instantiation thereof.

  44. Possibly bogus factoid: fruit fly sperm cells are about 20 times longer than the insect’s body. I invite anyone having first hand knowledge to support or refute.

  45. Allan Miller:
    DNA, the physical substance, is actually as much phenotype as genotype. More so, in many respects. Gene-centrism relates to the passage of sequential information down the generations and across populations, not to any particular physical instantiation thereof.

    This is the central question that Sal can’t get his head around. What is inherited across multiple generations of organisms? What changes to cause heritable differences between populations? The answer to both is something he appears not to like and consistently tries to deny, despite all evidence.

  46. petrushka:
    Possibly bogus factoid: fruit fly sperm cells are about 20 times longer than the insect’s body. I invite anyone having first hand knowledge to support or refute.

    Were you perhaps inspired by the new paper in Nature that attributes this actual fact to sexual selection?

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