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. Rumraket:
    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

    Hopefully your computer lets you search for files by time-of-creation?

  2. REW:

    DNA determines heritable features- DNA does determine the vast majority of them though.

    I can understand why you and most of the scientific community feel that way, but that is partly due to sampling and confirmation bias of accounting for only living working forms. We fail to include in the accounting the non-DNA changes that result in death, hence we don’t call them heritable changes, and then make the wrong inference then that there is no structural information in the non-DNA regions because there was no heritable change to observe.

    If we really thought DNA defines all heritable structural information, we ought to be able to throw an apple’s DNA into a yeast cell and expect apples to emerge eventually.

    We have the HeLa immortal cell line in labs taken from the ovaries of a cancer patient in the 1950’s. The “species” will not become human again. The full sufficient capacity to form limbs, organs, etc. is not in the DNA.

    So the way these questions will be settled will be by future laboratory techniques, assuming we’ll ever be able to make such techniques possible in light of the staggering difficulty of having to mutate several points in the cell simultaneously without recourse to changing the DNA. I linked to an article that shows the first steps toward doing that, but we’re a long way off from being able to reprogram the glycome “at will” while leaving the DNA alone.

    But we know that a functioning glycome is necessary for reproduction, and DNA is not a direct template for the glycome. Assuming for the sake of argument universal common ancestry is true and apple trees and tigers emerged from protists, it is evident the existing glycome for each species line needed to be in a state that is receptive to the next generation of DNA mutations. If this were not the case, we could grow apple trees from transgenic yeast. But since this is not the case, it shows the necessity of having the non-DNA components in a state that can cooperate with the DNA to make a living species. That state (be it the glycome, interactome, whatever) is not defined solely by the DNA as evidenced by differentiated cells in a multicellular creature.

  3. Here is one example of evidence that damage to the cytoplasm can create damage to development:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC21799/

    ABSTRACT Ever since x-rays were shown to induce mutation
    in Drosophila more than 70 years ago, prevailing dogma
    considered the genotoxic effects of ionizing radiation, such as
    mutations and carcinogenesis, as being due mostly to direct
    damage to the nucleus. Although there was indication that
    alpha particle traversal through cellular cytoplasm was innocuous,
    the full impact remained unknown. The availability
    of the microbeam at the Radiological Research Accelerator
    Facility of Columbia University made it possible to target and
    irradiate the cytoplasm of individual cells in a highly localized
    spatial region. By using dual fluorochrome dyes (Hoechst and
    Nile Red) to locate nucleus and cellular cytoplasm, respectively,
    thereby avoiding inadvertent traversal of nuclei, we
    show here that cytoplasmic irradiation is mutagenic at the
    CD59 (S1) locus of human–hamster hybrid (AL) cells, while
    inflicting minimal cytotoxicity. The principal class of mutations
    induced are similar to those of spontaneous origin and
    are entirely different from those of nuclear irradiation. Furthermore,
    experiments with radical scavenger and inhibitor of
    intracellular glutathione indicated that the mutagenicity of
    cytoplasmic irradiation depends on generation of reactive
    oxygen species. These findings suggest that cytoplasm is an
    important target for genotoxic effects of ionizing radiation,
    particularly radon, the second leading cause of lung cancer in
    the United States.

  4. stcordova: Here is one example of evidence that damage to the cytoplasm can create damage to development:

    …and it does that by creating reactive molecules that damage the DNA. But there certainly are examples that demonstrate what you’re suggesting : temporarily disrupting the cytoskeleton in just about any early embryo would trash development without changing the DNA.
    I think its good to think creatively about a field one is unfamiliar with as one learns, but suggesting that all of the experts don’t know what they’re talking about is just bizarre and demonstrates a spectacular inflexibility in ones thinking. As I said before I think this was a very good topic to bring up but I think its time you deferred to the experts ( i’m not talking about myself btw!)

  5. http://www.nature.com/nrm/journal/v11/n9/full/nrm2960.html

    http://www.nature.com.mutex.gmu.edu/nrm/journal/v11/n9/full/nrm2960.html
    [a quote from inside the paper]

    it energetically unfavourable for cells to rapidly manufacture organelles de novo, even in the case of organelles that originate from other intracellular compartments3, 6. Rather, a template-based biogenesis mechanism involving the growth and division of pre-existing organelles is the preferred method of maintaining organelle populations during cell proliferation. With each round of cell division, cells duplicate and apportion their various organelles to the two resulting cells with high accuracy, a process called organelle inheritance1.

  6. Here is an interesting article on organelle inheritance.

    I don’t have any background in cellular biology (ah another class to take), but this article points out the mitochondria are scattered in a cell with their won DNA. Is the DNA copied at each mitochondrial location? How can there be so little divergence in intra-cellular mitochondrial DNA after so many cell divisions if the mitochondrial dna between organelles is isolated?

    http://www.cell.com/cell/abstract/S0092-8674(00)81284-2

  7. From the National Academy of Sciences:

    The cytoplasmic organization may affect the expression of a trait without alteration in the genetic material (see Fig. C168). In Paramecia, the movement of the cortically located cilia may be oriented in the same direction. If a piece of the cortical cytoplasm is grafted in the reverse orientation, the graft will beat in the opposite direction and this ciliary movement pattern may be transmitted through generations.

    Similarly grafted vestibules may appear as an additional ingestatory apparatus in the progeny. These cortical layers contain no DNA or RNA. The pattern of development seems to be fixed within the organizational structure. epigenesis, non-Mendelian inheritance; Beisson J, Sonneborn TM 1965 Proc Natl Acad Sci USA 53:275.

  8. Increasing architectural and functional complexity likely came at the expense of the capacity to rapidly synthesize an organelle de novo. By de novo assembly, we mean the assembly of a new organelle in the absence of preexisting structures that comprise that organelle. Therefore, an acute selection pressure arose for accurate organelle inheritance such that progeny would not incur the energetically expensive cost of de novo organelle assembly (if indeed this was possible at all), which might prove deleterious, especially to a unicellular organism in a competitive environment. Just as with the genetic material, organelle inheritance proceeds via intimately coupled, sequential biogenesis (growth and replication), and partitioning (division) phases. Thus, just as with the DNA, organelles are duplicated and correctly apportioned between nascent daughter cells before completion of cytokinesis (Shima &
    Warren 1998).

    de novo organelle biogenesis in its purest sense is never
    required, as in all known cases organelles grow by proliferation and inheritance
    of preexisting organelles (Nunnari & Walter 1996, Lowe 2002).
    The templates that may govern their replication are inherited and endow progeny with a complete organelle complement. At most, de novo biogenesis may provide a fail-safe mechanism should organelles, for some reason, not be inherited correctly.

  9. Rumraket: Is there a point to this latest swathe of posts?

    Compared to the average ID journal, this site is top-tier. So this I imagine passes for publication and peer-review for Sal. He’s likely (and has admitted as much in the past) trying out the material he will be teaching to other students for his latest ID club so he can get feedback and knock off the stuff that even people who don’t know much about biology can see through.

  10. Is there a point to this latest swathe of posts?

    Yes, the posts and links support the OP that there is non-DNA structural inheritance!

    I provided evidence that organelle structure is inherited from pre-existing organelles, not solely from sequence information in the DNA — exactly as the OP claimed. I provided links to the actual lab experiments demonstrating the principles published in PNAS and Nature.

    Furthermore, in regard to organelle structural inheritance, it also shows redundant storage of structural information — meaning the organelles in a cell can provide parent structures for the organelles in daughter cells even if several of the parents get destroyed or injured.

    Cells with reduced numbers of organelles can synthesize sufficient numbers from pre-existing organelles if there are some still hanging around. This supports the OP.

    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.

    Hence, I also illustrated that in order to mutate non-DNA heritable features of an organelle (or whatever)– one has to mutate all the distributed copies of the information simultaneously (or at least force a bottle neck to one location), exactly along the lines of the OP.

    I highlighted a question regarding mitochondria which has DNA of its own. Each of the mitochondria duplicate semi-autonomously. This leads to some complication in how mitochondria in cells can evolve their structure and DNA given there are populations of mitochondria in a cell each with their own DNA and structure, not just a single mitochondria.

  11. I can’t believe I didn’t mention prions in the OP. That is a potential example in principle that structural properties are not necessarily inherited from sequence properties alone!!!!

    From a paper in the prestigious scientific journal Nature, 2012:

    http://www.nature.com/nature/journal/v482/n7385/full/nature10875.html?foxtrotcallback=true

    Prions are a common mechanism for phenotypic inheritance in wild yeasts

    The self-templating conformations of yeast prion proteins act as epigenetic elements of inheritance. Yeast prions might provide a mechanism for generating heritable phenotypic diversity that promotes survival in fluctuating environments and the evolution of new traits. However, this hypothesis is highly controversial. Prions that create new traits have not been found in wild strains, leading to the perception that they are rare ‘diseases’ of laboratory cultivation. Here we biochemically test approximately 700 wild strains of Saccharomyces for [PSI+] or [MOT3+], and find these prions in many. They conferred diverse phenotypes that were frequently beneficial under selective conditions. Simple meiotic re-assortment of the variation harboured within a strain readily fixed one such trait, making it robust and prion-independent. Finally, we genetically screened for unknown prion elements. Fully one-third of wild strains harboured them. These, too, created diverse, often beneficial phenotypes. Thus, prions broadly govern heritable traits in nature, in a manner that could profoundly expand adaptive opportunities.

  12. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2174540/

    We have established an in vitro system for the formation of the endoplasmic reticulum (ER). Starting from small membrane vesicles prepared from Xenopus laevis eggs, an elaborate network of membrane tubules is formed in the presence of cytosol. In the absence of cytosol, the vesicles only fuse to form large spheres. Network formation requires a ubiquitous cytosolic protein and nucleoside triphosphates, is sensitive to N-ethylmaleimide and high cytosolic Ca2+ concentrations, and proceeds via an intermediate stage in which vesicles appear to be clustered.
    …..

    Dog pancreas rough ER microsomes, yeast membranes and cytosol, and wheat germ cytosol were prepared as described by Walter and Blobel 1983, Panzner et al. 1995, and Prehn et al. 1990, respectively. Cytosol and membranes from rat or cow liver and cow pancreas were prepared essentially as described (Walter and Blobel 1983), except that the sucrose cushion was omitted. Rabbit reticulocyte lysate was from Promega.

    Formation of ER Networks In Vitro

    To form membrane networks, 10 μl of cytosol, 0.5–1 μl of the light membranes, and 0.5 μl of an energy regenerating system (1 mM ATP, 0.5 mM GTP, 20 mM creatine phosphate, 0.1 mg/ml creatine kinase) were mixed and incubated at room temperature for the indicated times (10–90 min). Afterwards, membranes were stained by pipetting 1 μl of the reaction mixture into a 2-μl drop of 0.1% (vol/vol) octadecyl rhodamine (Molecular Probes) in buffer A, and observed by fluorescence microscopy using an Axioplan II microscope (Zeiss) equipped with an Orca 12-bit cooled CCD camera (Hamamatsu Photonics). In the basic fusion reaction, cytosol was replaced with buffer A.

    There you have it, DNA only coded the proteins, but the seed for the structure was pre-existing Endoplasmic Rectilium material!

    To get an idea of what parts I have now established as 3D photocopied vs. inherited purely by the DNA, see the diagram below. Note, I have just linked to two papers establishing the Golgi and the Endo Plasmic Rectillium have structural inheritance outside the DNA. I’ve mentioned also the mitochondrion, but that has mtDNA, so that is a bit tougher to make the case.

    I could probably find stuff for the cytoskeleton as well! Not pictured are the centrioles, but I showed that centrioles have non-DNA inheritance. But you can see then, I’ve accounted for large parts of the cell already.

    Now I have stuff I can run by some researchers at the NIH when go there for biochemistry training starting in a few weeks. One of them is a specialist in the areas relevant to the papers I cited. Yay!

Leave a Reply