The Sugar Code and other -omics

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I’ve long suspected the 3.1 to 3.5 gigabases of human DNA (which equates to roughly 750 to 875 megabytes) is woefully insufficient to create something as complex as a human being. The problem is there is only limited transgenerational epigenetic inheritance so it’s hard to assert large amounts of information are stored outside the DNA.

Further, the question arises how is this non-DNA information stored since it’s not easy to localize, in fact, if there is a large amount of information outside the DNA, it is in a form that is NOT localizable, but distributed and so deeply redundant that it provides the ability to self-heal and self-correct for injury and error. If so, in a sense, damage and changes to this information bearing system is not very heritable since bad variation in the non-DNA information source can get repaired and reset, otherwise the organism just dies. In that sense the organism is fundamentally immutable as a form, suggestive of a created kind rather than something that can evolve in the macro-evolutionary sense.

We often hear of genomics, but there are other -omics. There is proteomics, transcritonomics, lectinomics, and who knows what else which fall under the vague heading of epiginomics. If there is an immutable epigenetic kernel for each created kind, then this kernel will resist macro evolvability (like say from bacteria to a eukarya).

There are about 215 cell types in the human, and even supposing an average of a mere 5 developmental stages for each cell type, that’s over a thousand different transcriptomes in the human. The ENCODE consortium tracks only 150 or so transriptomes, and most are for cell in the cancerous stage. Where is the information stored to decide how to dice, splice, rna-edit RNAs, and postranslationally change proteins? ENCODE tracks some of this epiginomic data, but it’s only the tip of the iceberg. In fact, it could be argued each of the 200 trillion cells in an adult human has a slightly different transcriptome and proteome.

What other information storage mechanisms are there aside from DNA? It would have to be fairly fault tolerant so that you can’t knock out large portions of the system, and the information can be re-covered, much like having 100 backup hard-drives. One, and likely not the only information storage device, is implemented by the sugar code.

This link describes how the pharmaceutical industry has invested already 300 million dollars related to the sugar code, and how a mere 3 hexoes has the specificity of about 30 bits ( log2( 10^9) ).

Information carrying capacity of the sugar code

Only God knows how all the information could be stored outside of the DNA complex, but we have hints that for sure there is lots of memory storage capacity outside the DNA. The memory stored through the sugar code might only be one of the many mechanisms through which information is stored in the cell.

Here is another paper:

Analysis of the genome and proteome assumes the focus of attention in efforts to relate biochemical coding with cell functionality. Among other chores in energy metabolism, the talents of carbohydrates to establish a high-density coding system give reason for a paradigmatic shift. The sequence complexity of glycans and glycan-processing enzymes (glycosyltransferases, glycosidases and enzymes introducing substituents such as sulfotransferases), the growing evidence for the importance of glycans from transgenic and knock-out animal models and the correlation of defects in glycosylation with diseases are substantial assets to portray oligosaccharides as code words in their own right. Matching the pace of progress in the work on glycoconjugates, the increasing level of refinement of our knowledge about lectins (definition of this term: carbohydrate-binding proteins, excluding sugar-specific antibodies, receptors of free mono- or disaccharides for transport or chemotaxis and enzymes modifying the bound carbohydrate) epitomizes the sphere of action of the sugar code (functional lectinomics). It encompasses, among other activities, intra- and intercellular transport processes, sensor branches of innate immunity, regulation of cell-cell (matrix) adhesion or migration and positive/negative growth control with implications for differentiation and malignancy. The Q & A approach taken in this review lists a series of arguments in a stepwise manner to make the reader wonder why it is only a rather recent process that the concept of the sugar code has taken root in deciphering the mechanistic versatility of biological information storage and transfer.

55 thoughts on “The Sugar Code and other -omics

  1. stcordova: There is more than just the DNA ACGTs to provide information and technology to make a human being.

    Remind me, what’s your point? How does any of this support ID? Even if some people are wrong about some things and you are right, does that support ID somehow? If so, how?

  2. Remind me, what’s your point?

    Refer to the OP, what I’ve posted supports it.

    Increased complexity and information richness is an embarrassment to evolutionists like Dan Graur, Ken Miller, Nick Matzke, Larry Moran, etc.

    Scientific discoveries that embarrass evolutionists helps the ID movement. I’ve pointed out the scientific discovery of the sugar code because it may even be more information rich than DNA. If so, we’ve only scratch the surface of what functional designs exist in biology.

    There is a paper coming out in Septemeber, 2015. Can’t wait to read it:


    RNA-binding proteins, in cooperation with non-coding RNAs, play important roles in post-transcriptional regulation. Non-coding micro-RNAs control information flow from the genome to the glycome by interacting with glycan-synthesis enzymes. Glycan-binding proteins read the cell surface and cytoplasmic glycome and transfer signals back to the nucleus. The profiling of the protein–RNA and protein–glycan interactomes is of significant medicinal importance.

    Scope of review

    This review discusses the state-of-the-art research in the protein–RNA and protein–glycan recognition fields and proposes the application of amino acid codes in profiling and programming the interactomes.

    Major conclusions

    The deciphered PUF–RNA and PPR–RNA amino acid recognition codes can be explained by the protein–RNA amino acid recognition hypothesis based on the genetic code. The tripartite amino acid code is also involved in protein–glycan interactions. At present, the results indicate that a system of four codons (“gnc”, where n = g — guanine, c — cytosine, u — uracil or a — adenine) and four amino acids (G — glycine, A — alanine, V — valine, D — aspartic acid) could be the original genetic code that imprinted “rules” into both recognition processes.

    General significance

    Amino acid recognition codes have provocative potential in the profiling and programming of the protein–RNA and protein–glycan interactomes. The profiling and even programming of the interactomes will play significant roles in diagnostics and the development of therapeutic procedures against cancer and neurodegenerative, developmental and other diseases.

    Protein–RNA interactome; Protein–glycan interactome; Amino acid codes; Computational profiling; Protein engineering; Cell developmental diseases

    Mathgrrl where are you? Bueller, Bueller?

  3. The following link has a lot of material cut and paste in a nice format from various sources. Many of the sources are not cited and it’s never clear when one paragraph is written by one author and the next by another (short of googling individual phrases).

    But it is an outstanding introduction into my hypothesis that DNA doesn’t contain all the information and technology to build a human which likely lies in the 3rd alphabet of life. If the hypothesis is correct, DNA is not central in importance but must share its significance with the Sugar Code.

    DNA contains information on how parts are built, but not all the information on how parts are to be put together.

    Some highlights:

    from Stephen C. Meyers book : Darwin’s doubt :

    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.


    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.

  4. Do you have a reference to this revelation from somewhere a bit more mainstream?

    Also, Sal, the phrase “body plan” is used many times in that quote. What do you understand by “body plan”? Can you name a specific body plan that you are sure could not be the product of an evolutionary process?

  5. To answer Kantian Naturalists objections to immutability of form, I have some additional scientific data. I wrote in the OP:

    Further, the question arises how is this non-DNA information stored since it’s not easy to localize, in fact, if there is a large amount of information outside the DNA, it is in a form that is NOT localizable, but distributed and so deeply redundant that it provides the ability to self-heal and self-correct for injury and error. If so, in a sense, damage and changes to this information bearing system is not very heritable since bad variation in the non-DNA information source can get repaired and reset, otherwise the organism just dies.

    I just found a paper supporting this through evolutionnews and views!

    First, Richard Dawkins gets something right:

    It is true that there are quite a number of ways of making a living — flying, swimming, swinging through the trees, and so on. But, however many ways there may be of being alive, it is certain that there are vastly more ways of being dead, or rather not alive. You may throw cells together at random, over and over again for a billion years, and not once will you get a conglomeration that flies or swims or burrows or runs, or does anything, even badly, that could remotely be construed as working to keep itself alive. (1987, p. 9)

    [I wonder if Richard ever gets called by the nickname for Richard?]

    But anyway that claim by Richard gets reiterated in a recent paper in Protein Science

    Unlike protein folding, self-assembly of the interactome has not yet prompted such widespread attention, and for understandable reasons. It is a problem of bewildering complexity…Where does one begin? Our goal here is to show that assembly of the interactome in biological real-time is analogous to folding in that the functional state is selected from a staggering number of useless or potentially deleterious alternatives.

    and the paper even repeats Jonathan Wells Humpty Dumpty reference, before unwittingly pointing out the immutability of form, bwahaha!

    …all the king’s horses and all the king’s men / couldn’t put Humpty together again.
    [O]ur calculations of combinatorial complexity [show] that the emergent interactome could not have self-organized spontaneously from its isolated protein components. Rather, it attains its functional state by templating the interactome of a mother cell and maintains that state by a continuous expenditure of energy. In the absence of a prior framework of existing interactions, it is far more likely that combined cellular constituents would end up in a non-functional, aggregated state, one incompatible with life…The spontaneous origination of a de novo cell has yet to be observed; all extant cells are generated by the division of pre-existing cells that provide the necessary template for perpetuation of the interactome.

    SEE! The mother cell as a whole, not just the DNA has heritable features that if sufficiently damaged, will not allow cellular replication. That means the interactomes of various species also have to evolve in ways that are functional at each step, but since there are only islands of functionality surrounded by oceans of non-functionality and death in the change of the interactome, transitionals are prevented, and there are basic immutable forms just like there are immutable forms for proteins — i.e.

    The forms are immutatble.

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