Complex Specified Information Without an Intelligent Source

Meyer claims that specified complex information can only arise from an intelligent source, justifying that claim by citing a series of examples. One of those examples is computer code. In my previous post, I suggested that this was not an adequate example because of fundamental differences between computer code and DNA information. An obvious question is whether there is an example of specified complex information that is not derived from an intelligent source but solely from physical or chemical functionality. In this post I would like to offer just such an example.

The magnificent example of antibodies was presented by Dr. Craig Story in the December 2009 issue of Perspectives on Science and Christian Faith, Vol. 61, No. 4, p.221. (if you aren’t a member or don’t have a subscription, copies are available from the ASA office for $10 plus shipping and handling; contact asa@asa3.org.) In his article, Craig explains how the immune system works, focusing on the importance of the inherent randomness in the process. In this post, I would like to offer a physicist’s interpretation of his paper, with a focus on the information content. Craig has graciously reviewed these comments and corrected my errors in biology.

Stem cells in our bone marrow continuously produce a population of pre-B cells, so called because they are precursors to B cells, which manufacture antibodies when mature. These pre-B cells are all identical and have the same antibody gene DNA. This population therefore has a relatively low information content. All the complexity is within the cell and there is no diversity in the population of cells. As the pre-B cell population prepares to moves into the body, the cells undergo a transition into B cells. In the process, key segments of DNA in each cell are rearranged randomly to form a unique and novel DNA sequence. The process is described in detail in Craig’s paper. It is a constrained process so that the resulting antibody protein is always a particular folded configuration that may have affinity to an antigen, but the gene segments are randomly rearranged and joined to alter the magnitude of the affinity. The result is a population of B cells, each one of which is different in terms of its antibody DNA. This means that we have a transformation of a low information population of pre-B cells to a high information population of B cells, with reference to their antigen-binding abilities. The complexity has increased dramatically but we do not yet have specificity.

As a B cell moves through the body, it may or may not encounter an antigen with which it has affinity. If it does not, the B cell dies and that particular configuration no longer exists in the body. However, if an antigen appears with which a B cell has some degree of affinity, the B cell will attach to the antigen. In this case, that B cell will reproduce through cell division to create clones of itself. This process occurs throughout the population of B cells with the result that only B cells with some affinity to the environment of antigens survive. This is a basic level of specificity.

There is another level of specificity that Craig describes. A first-responder B cell usually will have a relatively small degree of affinity to an antigen. As this cell reproduces itself, an enzyme enhances the mutation rate of only the portion of the antibody genes that determines the affinity. In some cases, mutation rates can reach as much as one nucleotide per cell division. This means that the subpopulation of this particular B cell grows with a dynamic diversity of various degrees of affinity to that antigen. The cells with the strongest degree of affinity will preferentially attach to the antigens, leaving those with weaker affinity without antigens and therefore a death sentence. Over time, this subpopulation will be predominantly one with strong affinity to this particular antigen. This, in a nutshell, is why vaccines work.

In the bigger picture, this example shows how a homogeneous population of pre-B cells is transformed to a dynamically diverse population of B cells, with a tremendous increase in information content. This complex information then becomes highly specified by fine-tuning to match the antigens to which they are presented. The result is a high degree of specificity and complexity with no involvement of an intelligent designer as an immediate cause. This does not, of course, preclude the sustaining involvement of an Intelligent Designer at a metaphysical level.

Craig points out the critical role of randomness as a key characteristic of the cellular processes involved in the immune system. The random process of gene rearrangement is necessary to ensure a sufficiently broad range of binding specificities, such that some of them are almost sure to bind to one part of each pathogen. His example also illustrates clearly how highly complex and highly specified information is derived directly from a population of relatively low-information cells. Hence, the argument that Meyer makes that all complex specified information comes from an intelligent source does not withstand scrutiny.

The antibody example is a beautiful illustration of the basic processes of evolution. It begins with the common ancestry of the stem cells that produce an ancestral population of pre-B cells that are essentially identical. Descent with random variability occurs in the generation of the B cells, which are all unique with respect to their antibody gene DNA. Natural selection describes the way in which B cells that do not bind to an antigen will die while those that do bind to an antigen proceed to reproduce clones. The random variability of the dynamically diverse population of antibodies ensures the formation, within a short period of time, of antibodies with affinity to virtually any antigen. The subsequent way in which those B cells acquire stronger affinity to that antigen is a type of adaptation. Darwin suggested that these basic processes, operating over a long period of time, could account for the origin of species. Little did he suspect that these very processes are active continuously in our bodies on a relatively short time scale to provide a vital line of immunological defense.

240 comments to Complex Specified Information Without an Intelligent Source

  • Charles Austerberry

    Dear Ide:
    Thanks for reading the reference, and for continuing the conversation.
    It is a complicated and confusing subject.
    Where the text notes that two mechanisms of diversification are “consequences of the recombination,” it is referring to the DNA recombination events that assemble variable region encoding DNA from V segments and J segments in the case of antibody light-chain encoding DNA, and from V, D, and J segments in the case of antibody heavy-chain encoding DNA.  One of these two “consequences of the recombination,”  junctional diversification, is probably worth your continued study, because it can result in new base pairs of DNA inserted into so-called “N regions.” These N regions created by junctional diversification encode hypervariable regions within the variable regions of the antibody chains.
    Somatic hypermutation, on the other hand, usually causes substitutions rather than insertions or deletions.  It’s a fascinating process whereby double-stranded breaks in DNA are repaired by somewhat error-prone DNA repair mechanisms.  It’s well-named.  It also happens much later, after the assembly of the V-(D)-J segments.
    I appreciate your sense that mutations of existing code differ from insertion of new code.  And as we both noted earlier, changing a DNA sequence (whether by insertion, deletion, or substitution) randomly differs from swapping DNA segments randomly.  All are important in evolution.  Natural selection selects for or against genomic changes of two basic types: 1) those arising from mutations (insertions, deletions, substitutions, and larger-scale rearrangements) and 2) those arising from sexual recombination (meiotic recombination and allelic assortment as gametes are formed followed by random combination of gametes when fertilization occurs).
    When is there “new code”?
    Well, one could limit the definition of “new” to only cases where the DNA (or RNA) becomes longer than it was previously.  “Origin of life” experiments that result in longer RNAs, insertional mutations, and many N regions in antibody gene junctional diversification would fit that definition.  These are analogous to new letters being typed in a text.
    One could also expand the definition to include point substitutions such as those occurring in germline mutations responsible for most human single nucleotide polymorphisms (SNPs) as well as somatic hypermutation in antibody encoding genes.   These are analogous to spelling changes in which a single letter is changed.
    One could further expand the definition to include rearrangements of existing DNA segments.  That would include DNA recombinations in meiosis, chromosomal translocations and inversions, and the V-(D)-J joining in antibody gene variable region assembly.  These are analogous to moving parts of words, whole words, or word phrases around in a text.
    And finally, one could further expand the definition to include new combinations of chromosomes, which happens through meiotic allelic assortment plus fertilization in the reproduction of sexual organisms, and which also happens when a particular light chain associates with a particular heavy chain in B cells making antibodies. These are analogous to exchanging paragraphs, chapters, or even books in assembling “new” books or libraries of books.
    Your choice to limit “new” to the very first definition (a longer sequence, with nucleotides not previously encoded in the genome) is fine with me, as long as we all understand the big picture.
    Cheers!
    Chuck
     
     
     

    • Charles Austerberry

      I need to correct something I wrote in this post.  I wrote: “Somatic hypermutation, on the other hand, usually causes substitutions rather than insertions or deletions.  It’s a fascinating process whereby double-stranded breaks in DNA are repaired by somewhat error-prone DNA repair mechanisms.”
      When I mentioned double-stranded breaks in DNA I was thinking of switch recombination, not somatic hypermutation.  Both are initiated by activation-induced cytidine deaminase (AID) in the heavy chain antibody-encoding DNA of B cells, but only switch recombination is known to involve double-stranded breaks.  Let’s get into switch recombination only if you want to; somatic hypermutation is more pertinent to the diversification of antigen-binding capability.
      In the case of somatic hypermutation,  DNA polymerases often causes mutations when replicating DNA upon which AID has acted.  In some cases, the deaminated base (being “wrong”) directly leads to a mutation when the DNA polymerase uses it as a template.  In other cases the deaminated base is removed by an enzyme called UNG, and it’s the base-lacking position in the DNA template that confuses DNA polymerase.  Finally, sometimes base excision repair (BER) or mismatch repair (MMR) follows the deamination, and both BER and MMR frequently make mistakes (more often in the antibody genes than elsewhere in the genome, for unknown reasons).  Here’s how a recent article summarizes it:
      “Several things can happen following AID-catalyzed C deamination. The resulting U opposite G upon normal DNA replication leads to C → T transitions. On the other hand, U can be removed by UNG, and the resulting abasic site, when copied by an error-prone DNA polymerase that can insert T or C opposite the lesion, causes C → A and C → G transversions. Alternatively, U can undergo MMR or BER, which, in the presence of error-prone polymerases, can yield various transitions and transversions.”
      The reference for this is:
      http://www.jbc.org/content/284/41/27761.abstract
      Cheers!
      Chuck
       
       

  • Charles Austerberry

    Just to clarify: different chromosomes do not leave or enter B cells in that last level I mentioned above.  What immunologists refer to as “allelic exclusion” simply means that only one of the light chain-encoding chromosomes,  and only one of the heavy chain-encoding chromosomes, are expressed in a given B cell.  It’s analogous to allelic assortment plus fertilization (sexual processes producing new combinations of chromosomes) in a sense, but only in a loose sense because the B cells still have the other, unexpressed chromosomes.
    Cheers!
    Chuck

  • Charles Austerberry

    Ide, note that I did not even include duplication of DNA in my list, because while duplication of genes followed by diversification is very important in evolution (including the evolution of the immunoglobulin superfamily of genes), to my knowledge duplication of DNA is not involved in the antibody gene assembly process happening within a maturing B cell (except for limited DNA replication as part of DNA repair).  Now by “gene duplication” I do not mean DNA replication prior to cell division.  Rather, I mean new copies of genes or other segments of DNA in a genome apart from replication of the entire genome.
    DNA replication prior to cell division is also important, of course, because a larger population of cells provides the raw material (multiple copies of DNA) in which diversification can happen.
    This is true within an individual’s immune system in multiple senses.  It’s true in the development and differentiation of various blood cell lineages in the bone marrow to give rise to (among others) diverse B and T cells.  It’s also true later when a particular B or T lymphocyte encounters antigen and become activated.  Immunologists specifically refer to this latter case as “clonal expansion.”
    We can extend these concepts to phylogenetic evolution too as long as we are speaking of the germline DNA that gets passed on to the next generation rather than somatic DNA (such as in B cells) which does not get passed on to the next generation.
    So to summarize, both gene duplication within a genome, and cell/organism reproduction, can provide multiple copies of DNA that can then diversify.
    I appreciate your sense that duplication of existing CSI differs from de novo production of CSI.  I’m only noting that duplication and replication are integral aspects of biological phenomena.
    Cheers!
    Chuck

  • Ide Trotter

    Chuck,
     
    Wow! And many thanks again.  I can’t pretend to have fully assimilated all that you have provided here.  I’m sure we are completely together that “duplication of existing CSI differs from de novo production of CSI.  I’m only noting that duplication and replication are integral aspects of biological phenomena.”
     
    In your earlier section on, “When is there “new code”? it seems most of the actions you bring to my attention fall into my “making use of old code category.”  However, “point substitutions such as those occurring in germline mutations responsible for most human single nucleotide polymorphisms (SNPs)” seems on first impression to be a different animal and possibly closer to what I would call “new.”  (Keep in mind that I’m learning here under your patient tutelage.) Anyhow, I went to Wikipedia and find that SNPs are generally discussed as defects leading to dysfunction.  I believe we have stipulated that we haven’t settled on a mutually agreed understanding of how best to define CSI. Nevertheless, I have a feeling that I would be unlikely to eventually agree that mutations leading to dysfunction represent the type of functionally constructive CSI on which life is based.  So I’m not inclined to think it is what I’m looking for.
     
    I hope to get your reaction to this thinking on my part before I go into recess.  But after that I’m afraid I’ll have to drop out of the discussion for a while.  We are about to have a family gathering (ten grandchildren, the 11th in China for the summer won’t make it, and assorted parents) buried so far in the Colorado mountains that our cell ‘phones don’t work and we are thankful to have slow dial up email.  I’ll be back playing catch-up around the middle of August.
     
    Thanks again for your patient instruction.  Your paying students are most fortunate to have a teacher like you.
     
    Ide

    • Jon Tandy

      Ide,

      I had wanted to reply to your last message to me on June 26 regarding some specifics on the examples I had given, to explain how I see CSI increasing in an information technology example, as one way to work back into the biological examples.  But I got buried in several things, and anyway I think Chuck’s comments to you on DNA really get closer to the kinds of details you have been looking for, and I wouldn’t want to get in the way of that conversation, given your limited time resources.

      And on the biology score, I certainly can’t claim to be able to contribute a great deal of in-depth knowledge.  However, let me comment at a bit of a high level response.  You seem to be grasping at any possible reason not to accept that genuinely new information might be created in biological systems, but seem to want to attribute new biological developments to the existing “pool of CSI”.

      You also suggest that duplication of existing code is in a different category from “new code” or “new CSI”.  I will just say that this is a non sequitur, whether you look at it from the point of view of biology or computer science.  I’ve written enough computer programs to know that you might be right, but not necessarily.  I can copy and paste existing code, with modifications, and create entirely different code with significantly different function.

      And in the biological realm, although far from my expertise, I would suggest that you need to look at this from the point of view of the biological evidence, rather than through the narrow lens of CSI.  Remember that ID advocates created the concept of CSI, but biologists are the ones doing the actual work in the field. 

      The fact is, biologists have some pretty good ideas about where novel features come from in the DNA.  It comes from point mutations, gene duplication, substitutions, and all the other things that Chuck has written about it.  These are random or semi-random rearrangements and modifications of existing DNA, that were in many cases not anticipated in the original sequence.  There is no intelligence directing these modifications, at least that we can observe in laboratory experiments (I certainly leave open the possibility of God guiding quantum and classical events through providential action, but that’s a matter of faith, not empirical evidence).

      So even if there are duplications of existing code, it doesn’t matter in the slightest that the DNA is reusing what you might term “existing CSI”.  The resulting functional features are in many notable cases NOT just copies of existing functionality, and are therefore truly novel features.  If we didn’t have the “Intelligent Design” paradigm in mind when looking at it, we would have to conclude that random modifications occur in DNA, which result in the development of new features that in some cases provide greater survival benefits. 

      Whether or not we put ID labels on this and frame the discussion around CSI, the facts are still the facts.  In this sense, I fail to see what ID actually contributes to our knowledge of biology.

      Jon

  • Charles Austerberry

    Dear Ide:
    Thanks again for your post, and for your gracious comments.  I enjoy learning and facilitating the learning of others, especially about biology, and you have been a patient and persistent correspondent, for which I am grateful.
    Regarding the SNPs: indeed, many are deleterious, and do cause disease, at least in some contexts.  Most seem neutral, as far as we can tell.  But many  can be advantageous, at least in some contexts (for just one example, in cultures raising livestock for milk, a mutation that causes continued expression of the lactase gene through adulthood would provide an advantage).  Many SNPs  provide benefit.
    The more I learn about somatic hypermutation and N-segment nucleotide insertion, for example, the more I am struck by the elegance of the immune system’s balanced use of random and nonrandom mechanisms to achieve remarkable function.
    My thanks to Craig Story, Randy Isaac, Jon Tandy, other posters, and you, Ide, for the discussion we’ve had.  Best wishes, Ide, for a wonderful family reunion!
    God bless,
    Chuck

  • [...] an intelligent source does not withstand scrutiny.The full explanation of antibody production is here, and the full argument against Signature of the Cell here. Both pages are maintained under the ASA [...]

 

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