Discovery Institute's Blog, page 505

Mike Behe to Tour UK

Click here to listen

CSC Senior Fellow (and sometime ENV contributor) Mike Behe is set to tour the United Kingdom starting this Saturday, speaking on "Darwin or Design? What does the science really say?" This week-long tour is sponsored by the Centre for Intelligent Design of the UK, and residents of Leamington/Warwick, London, Glasgow, Belfast, Cambridge, and Bournemouth should avail themselves of the chance to catch one of Dr. Behe's evening lectures there. He will also be the main speaker at a day long conference in Oxford.

Online registration is required. Visit http://www.darwinordesign.org.uk to register and for more detailed information.

What DNA Has to Tell Us About the Origins of Life

There's an outstanding review of Stephen Meyer's Signature in the Cell by Terry Scambray in the New Oxford Review, which highlights a bit of relevant history for the reader on both Dr. Meyer and Darwin's theory:

Signature in the Cell: DNA and the Evidence for Intelligent Design is a testament to the fact that, fortunately, such advice ["don't ask questions"] never sank in with Meyer. After abandoning his life as a geophysicist in search of oil for Atlantic Richfield, and then earning a Cambridge doctorate, he continued to ask questions as he humbly but resolutely began his new quest: the search to understand the origins and basis of life.

This is, of course, an ancient quest. From then to now, most people have believed that the sublime order that we see in nature must have been designed. But Charles Darwin argued that design was an illusion: Nature alone, by a process of accidental trial and error over eons of time, had produced this ineffable harmony.

Despite the fact that Darwin's theory of natural selection was accepted by most educated people, the theory itself was weakly supported from the beginning. It gained acceptance mainly for cultural rather than scientific reasons. Progressive ideas had gained dominance by the nineteenth century; correspondingly traditional institutions -- mainly religion -- were taking their lumps. Against this background, criticisms of Darwin were castigated as regressive and religiously motivated, despite their scientific objectivity and rigor. Such polemical treachery continues to this day.

In this sense, Meyer's sweeping compendium provides a final, annihilating assault on the Darwinian Po temkin village. That his remarkable treatise should be published in 2009, which is both the 200th anniversary of Darwin's birth and the 150th anniversary of The Origin of Species, adds a rounded finality to this destructive Darwinian episode in Western history.

Traveling to strange, exotic places profoundly influenced the visions of both Darwin and Meyer -- Darwin to South America, Meyer to the interior of the organic cell. Though in his adventures Darwin saw the great prolixity of life, he had no idea of the microscopic complexity within each cell, of which we have trillions in our bodies. To him, cells were mere blobs of protoplasm, blunt instruments like building blocks. But for Meyer and modern science, cells are dauntingly complicated and provide the basis for life.

Continue reading here.

BioLogos Voices Sing the Same Old Tune

I normally do not respond to criticisms and reviews of my work that are simply posted on the internet. Rather, I engage reviews, comments, and articles that appear in journals or prominent newspapers and magazines. The reason is that those printed venues usually ask noted scientists or philosophers to review books, so that they are very likely to contain the most pertinent and insightful comments. After all, if a book challenging Darwinian evolution is reviewed separately by the likes of Sean Carroll, Jerry Coyne, Michael Ruse, and Richard Dawkins, then the odds are good that they would have discovered any major errors, if such there be. However, if upon considering their criticisms, we see huffing and puffing instead of reasoned argument, or an attack on straw men instead of the actual arguments the author made, then we can conclude that the best minds in the field don't have answers to the arguments the book presents. And if the best minds don't have answers, it is quite likely that no one else has answers either.

That's what happened when The Edge of Evolution was published in 2005. It received uniformly hostile reviews by prominent Darwinists. However, in my author's blog on Amazon.com, at the time I engaged their criticisms and showed that virtually all of the reviews consisted of various degrees of bluster, question-begging, or attacks on straw men. What valid points remained I showed were minor and did not affect the main argument of the book: that while Darwinism can explain minor changes in life, there are strong reasons to think it does not explain much of the phenomenal complexity of the cell. Anyone who wishes to read those responses can do so at my blog and make their own judgments.

Normally I don't respond to internet criticisms, but sometimes I do. Recently several people have asked me to comment on a series of posts by "various guest voices" at BioLogos, a website promoting "theistic evolution." Lately the voices have taken quite an interest in my work, and all seem to be of one voice in finding it misleading, sub-par, and downright wrong (although I must say that they are always very polite when they accuse me of misleading people.) One of the voices is a member of the staff of BioLogos, and another voice is a biology student at the college where the president of BioLogos teaches biology.

The only voice that doesn't seem to have a pretty direct connection to BioLogos is a man named David Ussery, who is an associate professor of comparative microbial genomics at the Center for Biological Sequence Analysis at the Technical University of Denmark. I first met Dave in 1998 at Roanoke College in Virginia, where we debated my 1996 book Darwin's Black Box in front of a student audience. I immediately liked him -- a congenial man who shared my interest in DNA structure. Because Dave is the most senior scientific voice in the chorus, and because he is not affiliated with BioLogos, I will briefly respond to his ongoing review of The Edge of Evolution in two forthcoming posts. (As I write this he is up to four longish posts and apparently continuing; I won't be responding to any subsequent posts in the BioLogos series.)

The Darwinian Basis of the Prokaryote-to-Eukaryote Transition Collapses

The question of the evolution of eukaryotic cells from prokaryotic ones has long been a topic of heated discussion in the scientific literature. It is generally thought that eukaryotes arose by some prokaryotic cells being engulfed and assimilated by other prokaryotic cells. Called endosymbiotic theory, there is some empirical basis for this. For example, mitochondria contain a single circular genome, carry out transcription and translation within its compartment, use bacteria-like enzymes/components, and replicate independently of host cell division and in a manner akin to bacterial binary fission.

Despite such evidence, however, when assessing the causal sufficiency of unguided processes, they -- predictably -- come up short. After all, it is all-too-easy to lapse into a long-discredited Lamarckian "inheritance-of-acquired-characteristics" mentality. It is important to bear in mind that, even if a cooperative assemblage of prokaryotes did by some fluke of luck arise, such an arrangement is of no evolutionary significance unless there is a genetic basis to ensure its propagation.

A second problem with this scenario is that mitochondria use a slight variation on the conventional genetic code (for example, the codon UGA is a stop codon in the conventional code, but encodes for Tryptophan in mitochondria). This implicates that the genes of the ingested prokaryotes would need to have been recoded on their way to the nucleus. The situation becomes even worse when one considers that, in eukaryotic cells, a mitochondrial protein is coded with an extra length of polypeptide which acts as a "tag" to ensure that the relevant protein is recognised as being mitochondrial and dispatched accordingly. The significant number of specific co-ordinated modifications which would be required to facilitate such a transition, therefore, arguably make it exhibitive of irreducible complexity.

A few weeks ago, a review paper was published in the prestiguous journal, Nature, by the internationally renowned scientists and authors, Nick Lane and Bill Martin.

The abstract reports as follows:

All complex life is composed of eukaryotic (nucleated) cells. The eukaryotic cell arose from prokaryotes just once in four billion years, and otherwise prokaryotes show no tendency to evolve greater complexity. Why not? Prokaryotic genome size is constrained by bioenergetics. The endosymbiosis that gave rise to mitochondria restructured the distribution of DNA in relation to bioenergetic membranes, permitting a remarkable 200,000-fold expansion in the number of genes expressed. This vast leap in genomic capacity was strictly dependent on mitochondrial power, and prerequisite to eukaryote complexity: the key innovation en route to multicellular life.

The paper's chief concern is with regards to the energy costs of what they describe as "the most intense phase of gene invention since the origin of life." The problem is that bacterial cells are highly unlikely to possess the technology necessary to facilitate such a transition.

How is one to resolve this paradox? The authors explain:

The answer, we posit, resides ultimately in mitochondrial genes. By enabling oxidative phosphorylation across a wide area of internal membranes, mitochondrial genes enabled a roughly 200,000-fold rise in genome size compared with bacteria. Whereas the energetic cost of possessing genes is trivial, the cost of expressing them as protein is not and consumes most of the cell's energy budget. Mitochondria increased the number of proteins that a cell can evolve, inherit and express by four to six orders of magnitude, but this requires mitochondrial DNA. How so? A few calculations are in order.

The paper's authors then present a discussion of the energy costs associated with the processing of eukaryotic DNA, and find that this value is far greater than that which can be produced by a bacterial cell. They thus conclude that the ATP required for the processing of eukaryotic DNA necessitates the presence of mitochondria, the powerhouse of eukaryotic cells.

Moreover, this mitochondrion needed to contain just the right set of genes and possess just the right gene density. The mitochondrion also required thousands of copies of the said genes, with each copy located in close enough proximity to the respective machinery such that the required energy could be produced at a fast enough rate.

The authors conclude by saying,

The transition to complex life on Earth was a unique event that hinged on a bioenergetic jump afforded by spatially combinatorial relations between two cells and two genomes (endosymbiosis), rather than natural selection acting on mutations accumulated gradually among physically isolated prokaryotic individuals. Given the energetic nature of these arguments, the same is likely to be true of any complex life elsewhere.

It gets worse, of course. Even if one presumes a sufficient supply of ATP from mitochondrial processes (such as oxidative phosphorylation and the electron transport chain), no traction is given to the causal sufficiency of undirected mechanisms in accounting for the origin of novel genes and proteins which are required for eukaryotic life. One might just as easily say that purchasing a bigger power supply for your computer will cause the computer to magically be programmed to perform more complex calculations and activities! Obviously, such power would be useless without the input of novel programming script -- information -- to appropriately harness the available power.

The paper describes the invention of new protein folds in eukaryotes as being "the most intense phase of gene invention since the origin of life." The problems associated with the chance-based origin of novel genes is only accentuated by the bioenergetic dilemma described here. Granting a satisfaction of the energy demands required for those new genes and protein folds, does neo-Darwinism gain any traction? It seems very clear that it does not.

Adaptive Immunity: Darwinism in Miniature or High-Tech Tinkering with Stasis?

[Editor's Note: Today we present part five out of six in a series by microbiologist Donald L. Ewert. These posts are responding to the BioLogos Foundation's blog where Kathryn Applegate argued that "random" processes that generate antibodies illustrate the creative power of Darwinian evolution. Previous installments of Dr. Ewert's rebuttal can be found at the following links: Part One, Part Two, Part Three, and Part Four.]

Kathryn Applegate's main point is that if "natural" processes -- which she characterizes as "random" and "blind" -- can be used to generate antibodies, the same mechanisms presumably could be used to "create life over long periods of time."

The question addressed here is: Do the terms "random" and "blind" accurately describe the mechanisms for generating diversity via V(D)J rearrangement and affinity maturation by SHM? Based on our current knowledge about antibody development, briefly described above, I contend that what may appear to be a random process is actually highly orchestrated at many different levels -- organismal (developmental), tissue (lymphoid tissues), cellular (B cells, helper T cells, antigen presenting cells), protein (MHC, enzymes, transcription factors, cytokines) and genetic (C and G placement, chromosomal accessibility). The function and structure of these highly specialized components must be coordinated to produce a specific antibody in response to an antigenic challenge. Independent developmental programs of the cell lineages, tissues, and organs must be controlled to ensure that their location and structure permit the interactions required for development of the B cell and antibody production. Therefore the combined functional and developmental aspects of antibody production involve a hierarchal matrix of regulatory controls that orchestrate the entire process. Antibody development is certainly not a "blind" or "random" process. What on the surface may seem like a random process is in fact an elegantly designed and regulated process.

Applegate's approach to these complex mechanisms is an example of a reductionism that has dominated the field of biology, including evolutionary biology, for over a century. By focusing on the narrow aspects of structure and function, the context that operates to control and integrate them in an organism is overlooked. When viewed as a system, the highly complex, integrated and regulated operation of the immune system bears little resemblance to the undirected, blind processes that are theorized to drive Darwinian evolution.

What is "natural"?

Applegate argues that the processes of G.O.D. and affinity maturation involve the same "natural" processes involved in Darwinian evolution, i.e., undirected random mutations resulting in variable phenotypes that are selected based on their survival advantage. On the surface her narrow comparison may seem reasonable, but from the vantage of systems biology the process is anything but "random." The mutations in question are not randomly dispersed throughout the genome but directed to regions within the V gene segments. Moreover, the process of G.O.D. is regulated at every step during BCR development. The entire process is programmed to achieve the goal of antibody production, and to prevent B cell lymphoma and autoimmunity. Purportedly, Darwinian evolution has the ability to produce new biological features. But no new novel structures are ever produced in this process as evidenced by the fact that sequence analysis and computer modeling show that the binding site (V) regions of the immunoglobulin genes of humans are similar to the most evolutionary distant vertebrate species, sharks (Marchalonis et al.). Furthermore, the intricate systems that control the development of antibody diversity are just as "natural," and can provide greater insights for research on how living systems are designed to adapt to change.

The processes involved in BCR development in fact are not analogous to the Darwinian evolutionary model but rather suggest the work of a programmer who developed a complex program to sustain and protect the biological integrity of each organism in a constantly changing environment.

Implications: Change has limits

Any scientist committed to the pursuit of truth must follow the evidence where it leads. Can the elegant processes that regulate antibody development provide insights for how living organisms may be designed to adapt to changes in the environment? Melvin Cohn recently commented in the affirmative: "In my view, it is by revealing the elements and principles of somatic evolution that comparative immunology will some day have its greatest impact on biological thinking." (Cohn, 2006)

If we take the data from the immune system at face value, a principle emerges: biological change is orchestrated within limits. The ability to both anticipate (generation of Ig diversity) and adapt (affinity maturation) to changes in the environment while maintaining the integrity of the system is likely a designed feature of organisms. Such change is anticipated to be limited to strategic sites in the genome, allowing the organism to adapt to its environment while maintaining its integrity. A recent paper by Li et al. provides evidence that the mechanism of targeting mutations found in Ig V gene hypermutaion may be deployed more generally to affect adaptations in other biological systems:

One of the most striking findings in our present study is that not only in the antibody-combining site but in other protein-protein interfaces almost all of the affinity-enhancing mutations are located at the germline (mutation) hotspot sequences (RYYW or WA)... (Li, 2010)

Their findings indicate that protein-protein interfaces which are important in the regulation and establishment of macromolecular complexes and networks use the same basic strategy to target sites of plasticity. Thus the strategic placement of mutation hotspots may be a design feature of many functional and structural elements of biological systems that allow organisms to adapt to internal and environmental changes.

This concept of bounded change also predicts that the essential characteristics which distinguish higher taxa will remain stable and be evident in the comparison of extant species with organism in the fossil record. Stephen Jay Gould and Niles Eldredge reported in 1977 that stasis is a dominant feature of the history of most fossil species. More recently, Lönnig and Saedler, in a review article in Annual Reviews of Genetics, stated that "the richness and often extraordinary quality of the fossil record ... leave no reasonable doubt in the minds of most qualified observers as to the existence of stasis."

Ironically, the molecular mechanisms found in the regulation of BCR development, rather than supporting a theoretical model of unguided evolutionary change, as Applegate proposed, may provide insights into how stability is maintained on the level of higher taxa while allowing for adaptation and limited diversity within taxonomic limits.

References

Cohn M, 2006. "What are the commonalities governing the behavior of humoral immune recognitive repertories?" Developmental and Comparative Immunology 30: 19-42.

Fuxa M and Skok J. 2001, "Transcriptional regulation in early B cell development." Current Opinion in Immunology. 19: 129-136.

Gould S and Eldridge N, 1977. "Puncturated Equilibria: the tempo and mode of evolution reconsidered." Paleobiology 2:115-151.

Hansen, JD and McBlane, JF. 2000. "Recombination-Activating Genes, Transposition, and the Lymphoid-Specific Combinatorial Immune System: A Common Evolutionary Connection." Origin and Evolution of the Vertebrate Immune System. Edited by L. Du Pasquier and G. W. Litman. Berlin, Springer. 248: 111-135.

Li B, Zaho L, Wang C, Guo H, Wu L, Zhang X, Qian W, Wang H, and Guo Y. 2010. "The protein-protein interface evolution acts in a similar way to antibody affinity maturation." J. Biological Chem. 285:3865-3871.

Lönnig W-E and Saedler H. 2002. "Chromosome Rearrangements and Transposable Elements." Annu. Rev. Genet. 36: 389-410.

Marchalonis JJ, Jensen I, and Schluter SF. 2002. "Structural, antigenic and evolutionary analysis of immunoglobulins and T cell receptors." J Mol Recognit. 15: 260-271.

McBride KM, Gazumyan A, Woo EM, Schwickert TA, Chait BT, and Nussenzweig MC. 2008. "Regulation of class switch recombination and somatic mutation by AID phosphorylation." Journal of Experimental Medicine. 205:2585-2594.

Nutt S and Kee B. 2007. "The Transcriptional Regulation of B cell lineage commitment." Immunity 26: 715-725.

Zheng N-Y, Wilson K, Matthew J, and Wilson P. 2005. "Intricate targeting of immunoglobulin somatic hypermutation maximizes the efficiency of affinity maturation." J. Exp. Med. 201:1467-1478.

Not By Chance: Controlling Affinity Maturation

[Editor's Note: This is part four of a six-part series from microbiologist Donald L. Ewert responding to Kathryn Applegate, of the BioLogos Foundation, in her arguments that the vertebrate adaptive immune system illustrates the claimed creative the Darwinian mechanism. Previous parts of Ewert's response can be found at the following links: Part One, Part Two, Part Three.]

Pathogen-directed activation of the immune response

The initiation of an immune response is designed so that the cellular and molecular components that are best equipped to deal with a pathogen are engaged. There are basically three response pathways. Non-protein antigens that have repeating carbohydrate units on their surface, such as are found on bacteria, can directly activate B cells. These B cell do not go through affinity maturation or class switch since multiple binding sites on the antigen make a strong bond with the B cell and the IgM class of antibody that is produced which has five receptors per molecule.

Responses to protein antigens fall into two classes, depending on whether the pathogen is intracellular or extracellular. Since intracellular antigens such as viruses are not accessible to circulating antibody, they activate cytotoxic T lymphocytes that are best equipped to kill them. This activation is directed by the Class I MHC antigen that is attached to the antigens as they are processed in cells. Extracellular proteins, which are best dealt with by circulating antibody, activate B cells to begin the process of affinity maturation and class switch that leads to the production of a monomeric IgG class of antibody. This latter pathway requires the assistance of a class of T lymphocytes called T helper cells (TH) and the interaction of Class II MHC proteins.

The collaboration with the TH cells at this stage of B cell development is critical to insuring that the antigen it has detected is indeed foreign and not one of the host organism's proteins. The B cell obtains confirmation to proceed by packaging or "presenting" a part of the antigen it recognized in a Class II MHC molecule for the T lymphocyte to "look" at. If the antigen receptor of the T lymphocyte, the TCR (which was also generated by V(D)J recombination), recognizes this antigen-MHC complex on the surface of the B cell, it in turn signals back to the B cell telling it to further differentiate into a plasma cell which produces the antibody protein, i.e., the cell-free form of the BCR. This double-key confirmation process prevents false starts, conserves energy, and reduces the risk that antibodies will be made against "self" antigens.

Subsets of TH cells are able to direct the production of specific classes of antibodies by B cells depending on the type of antigen. TH1 cells direct the production IgG antibodies that promote the ingestion and killing of microbes whereas TH2 cells direct the production of the IgE class of antibodies to pathogens such as helminthic parasites which are too large to be ingested by macrophages. The IgE coats the helminthes for destruction by eosinophils. This specialization of the adaptive immune response is not a random process and involves a matrix of intracellular and extracellular proteins that communicate information between the cells.



How do cells and pathogens find each other?

At the cellular level, as noted above, the process is initiated by the independent recognition of an antigen by two different classes of lymphocytes, a B cell and a T cell, each of which has an independent history of development that prepares them to cooperate with each other and regulate the immune response. This ensures that any potential B cell antigen (at least for T cell-dependent antigens) is confirmed by at least two antigen receptors before the immune system commits to producing high affinity class-switched antibodies. It is thus essential that these two lymphoctes, both of which have bound to the same pathogen, are able to find each other. With several million B and T cells distributed throughout the body, this is no simple task . While the chances of two cells encountering the same antigen and then coming together are very small, the activated B and T cells are programmed to release specialized proteins (chemokines) that attract one another within the confines of particular compartments found within lymphoid organs (lymph nodes and spleen). If these encounters were left to chance alone, the adaptive immune system could not mount a response in time to defend the host against a proliferating pathogen.

Controlling the destructive effects of AID

At the molecular level, SHM utilizes highly dangerous enzymes to make un-templated changes at very precise regions of the DNA. SHM is initiated by an enzyme, activation-induced cytidine deaminase (AID), which deaminates cytidine residues in single-stranded DNA that are exposed during Ig gene transcription. The resulting mutations (uridine/guanine mismatches) are then processed by mismatch repair enzymes and error-prone polymerases that normally correct errors in the DNA. In this case, however, they cause point mutations and substitutions to increase. The latter effect is the result of a pre-programmed subversion of a natural repair process, as will be discussed below.

Due to AID's potential to alter the information contained in the genome, its expression is highly regulated and targeted to specific regions in the antigen-combining site of the immunoglobulin gene called the complementarity-determining region (CDR). A recent paper by McBride et al. identified several levels of AID regulation, concluding:

Thus, AID appears to be controlled by multiple potentially overlapping mechanisms. We speculate that this type of combinatorial regulation facilitates fine control of AID level, which is required because small imbalances in its expression can result in catastrophic effects on genomic stability.

Control of AID activity is important for the following reasons:

First, it is essential to cause only subtle changes that alter the affinity the BCR for the antigen, but not the specificity of the antigen-combining site. AID induced changes are targeted to sites in the CDRs of the V region that form the antigen-combining site, when the protein is folded. These changes slightly alter the amino acid composition of the receptor, changing its affinity for the antigen. Other regions of the V gene that form the scaffolding for the V region, called framework regions (FWR), have a low mutation rate. Mutations in the FWR would damage the structure of the antibody and cause the B cell to initiate a program of cell suicide called apoptosis.

Second, the V region which contains the CDR genes is adjacent to the constant region gene segments, which are the business end of the immunoglobulin gene. The constant region of the antibody must reliably interact with other components of the immune system (Fc receptors) to execute destruction and removal of a pathogenic agent. Therefore, this region must be spared from genetic changes to preserve the ability of the antibody-activated effector mechanisms that destroy a pathogen.

Third, enzymes like AID that alter the genetic code have the potential to wreak havoc on the information contained in the genome. Therefore, their activity must be regulated to preserve the integrity of the organism. It is remarkable that mutations can occur at an exceptionally high rate to effect a positive improvement in a specific region of the antibody but be controlled so as not to damage the B cell's ability to survive and proliferate.

Enhancing mutations by subversion of DNA repair enzymes

The molecular mechanisms involved in SHM have only recently been discovered. The targeting of the hypermutation mechanism involves two steps that determine the location and frequency of preserved mutations. The initial step targets the AID to specific sites (called mutation hotspots) that support formation of mutations in CDRs while minimizing mutations in the FWRs. This is not a random process. The next step, following the introduction of AID mutations, is the activation of DNA repair enzymes (DNA polymerases) that normally repair the damaged (deaminated) nucleotides. However, due the intricate positioning of the C and G nucleotides in the V region, the enzymes' repair activity is subverted, making the changes permanent in the CDRs and leading to an increase in the number of mutations (Zheng et al).

The intricate nature of the regulatory control of this process is presented in a paper by Zheng et al. in which they identify nine special features of IgV genes that "precisely regulate SHM while retaining a functional amino acid sequence."

Evidence is presented that IgVH genes have evolved to support the initiation of SHM by AID, but to minimize the occurrence of C-to-T-induced amino acid replacements through intricate positioning of coding strand Cs.

The complexity of these evolved biases in codon use are compounded by the precise concomitant hotspot/cold-spot targeting of both AID activity and the errors typical of Pol to maximize the accumulation of mutation in the CDRs and minimize mutations in FWRs.

(Zheng et al., emphasis added. Note that the gratuitous use of the adjective "evolved" was not supported in this or any other referenced research report.)

Who or What Plays the Music of DNA?

As I was driving in to work, the local NPR station had on an interview with a guy who's involved with gathering billions of seeds of various plant varieties into a "doomsday vault." It is on a remote Norwegian island and intended as a precaution against the presumed devastations of global warming. There were few surprises in the conversation -- the grim mood was well suited to the NPR target audience, which eats this stuff up -- apart from one rather interesting question from a listener. The guest, Cary Fowler of the Global Crop Diversity Trust, was asked why his group bothers with seeds. In the future, won't we be able to reconstitute life from the digital code of DNA?

Not necessarily, explained Fowler. He offered a few cryptic but telling comments about the complexities of gene expression, and how simply knowing the DNA sequence of a plant (or animal) may never be sufficient to generate life. Why? Part of the answer, implying a strong challenge to materialist explanations of life's evolution, is suggested in a recent and illuminating essay, "Getting Over the Code Delusion," in the Ethics and Public Policy Center journal, The New Atlantis.

Rare is the technical if otherwise quite accessible article that gives chills like this one does. Steve Talbott, a senior researcher at the Nature Institute, takes aim at the still-widespread illusion that DNA maps the construction of a living creature. In a 1992 essay, Nobel Prize-winning geneticist Walter Gilbert crowed that the time will come when a person will be able to say, of a human DNA sequence inscribed on a computer disk, "Here is a human being; it's me!" How utterly naïve that has since been revealed to be.

Richard Dawkins calls DNA "a remarkable feat of digital information technology," on the model of a computer albeit one that programs itself. Yet the burden of Talbott's article is to show why the whole computer metaphor is inadequate. If you want a better one, the really apt metaphor would be drawn from the art of dance -- or I'd say, music -- with all that implies by way of purpose, agency, and expression.

Linearly conceived DNA coding by itself doesn't suffice -- nowhere near so -- to orchestrate the building of proteins from amino acids, never mind a fully formed living creature. The study of the additional, inheritable information that's needed is called epigenetics. Where does that information reside? You might innocently picture the added information (epi- means "over" or "above") like a document you slip into a book on your bookshelf. It's a supplement to the book, over and above what's bound between the covers. To access the added information, it is just a matter of finding the right book on the shelf and opening it up. But this is totally wrong.

From Talbott's description, I am not sure that the word "information" really captures it either. What's at issue is gene expression -- when a given gene will be "expressed," or activated for translation into RNA and proteins, and when it will be unexpressed, or quiescent. Don't picture something simple and mechanical here like a player piano that "plays itself" by unspooling a roll of pre-perforated paper.

Driven by various "yet unknown signals and forces," arranging itself into incredibly tight, intricate and synchronized geometries "that researchers have yet to visualize in any detail," the chromosome is "engaged in a highly effective spatial performance. It is a living, writhing, gesturing expression of its cellular environment....The chromosome, like everything else in the cell, is itself a manifestation of life, not a logic or mechanism explaining life....[I]t's hard to ignore the active principle -- some would say the agency or being -- coordinating the movements."

Talbott writes of the way gene expression is "choreographed" through, for example, the behavior of the nucleosomes on which DNA is spooled, mediating between "gene and context -- a task requiring flexibility, a 'sense' of appropriate rhythm, and perhaps we could even say 'grace.'"

With our long-habituated reductionist, mechanistic expectations, we assume that if you dig deep enough into the organization of life, you will come across something like the ultimately dead mechanism of the self-playing piano. What you find instead is that "Things do not become simpler, less organic, less animate. The explanatory task at the bottom is essentially the same as the one higher up."

Thinking of the cell as running software, while accurate at the level of DNA -- and deadly to Darwinism all by itself since software implies authorship -- gives us only part of the story. Molecular biology has written "'finis' to the misbegotten hope for a non-life foundation to life, even if the fact hasn't yet been widely announced." Rather than a player piano, it is as if a piano were being played by a skilled and sensitive musician -- say, an improvisational jazz pianist -- with the instrument itself responding to his touch not as the expression of an algorithm but of its own life force. There is a very minimal musical score, in the form of DNA, inadequate to describe the music being performed, and then there is the pianist himself engaged in an improvisation on a swiftly shifting suite of themes.

And this is only the construction of proteins we're talking about. It leaves out of the picture entirely the higher-level components -- tissues, organs, the whole body plan that draws all the lower-level stuff together into a coherent, functioning form. What we should really be talking about is not a lone piano but a vast orchestra under the directing guidance of an unknown conductor fulfilling an artistic vision, organizing and transcending the music of the assembly of individual players.

Neo-Darwinism, to retain any credibility at all, requires the reductionist picture of DNA as the player-piano score of a clanking, whirring dead machine. In the modern Darwinian myth, chance variations in the dead code are what creates the raw material on which the zombie-like process of natural selection performs its blind, mindless work. If life ultimately reflects life -- "relations, movement, and transformation," as Talbott puts it, expressing purpose and agency -- down to the lowest level of organization, this represents a huge, seemly insurmountable problem for materialism.

Recapping Responses to Nature's Evolution Evangelism Packet

I've received quite a bit of positive feedback about the responses to the Nature 15 Evolutionary Gems packet that we've been responding to since last summer. As a recap of this series, below are links to the 9 parts responding to what I've affectionately called "Nature's Evolution-Evangelism Packet." Also, we've compiled the responses into a single PDF that can be used for educational purposes:

Part 1: Evaluating Nature's 2009 "15 Evolutionary Gems" Darwin-Evangelism Kit

Part 2: Nature's Microevolutionary Gems Part 1: Lizards, Fish, Snakes, and Clams

Part 3: Nature's Microevolutionary Gems Part 2: Bird-Sized Evolutionary Change

Part 4: Nature's Microevolutionary Gems Part 3: Flea and Guppy-Sized Evolutionary Change

Part 5: Nature's "Gems": Microevolution Meets Microevolution

Part 6: Evolutionary "Gems" or "Narrative Gloss"?

Part 7: Muscling Past Homology Problems in Nature's Vertebrate Skeleton "Evolutionary Gem"

Part 8: Of Whale and Feather Evolution: Nature's Two Macroevolutionary Lumps of Coal

Part 9: Evolutionary Biologists Are Unaware of Their Own Arguments: Reappraising Nature's Prized "Gem," Tiktaalik

Be sure to download the full PDF here.

Phillip Johnson on Dogmatic Signs

This month's edition of Touchstone Magazine has a great column by the godfather of intelligent design, Phillip Johnson, offering his review of Stephen Meyer's Signature in the Cell and his take on why the book has been met with such an uproar in the blogosphere:

In another way, however, it is peculiar that there is such a furious and often ill-informed objection to a learned volume that isn't even about the theory of biological evolution. The book advances well-reasoned arguments based on solid evidence about a prior problem -- the origin of the cell's information content -- concerning which most scientists would concede that they know very little.

The one thing that many of these scientists think they do know for certain is that, however the cell may have originated, the process could only have involved natural (i.e., unintelligent) causes. But this conclusion is not something these scientists know from the evidence. On the contrary, it is something they know--or rather, think they know -- regardless of the evidence. For a long time, it has been the rule in evolutionary science that, if the evidence does not support a fully naturalistic theory about both the origin of life and its subsequent development, then there must be something wrong with the evidence rather than with the theory or its underlying philosophy.

Johnson goes on to cite the powerful response to critics of SITC, Signature of Controversy :

The profoundly biased scientific and intellectual context into which Signature in the Cell was introduced is as important and fascinating a subject as Meyers' book itself. To understand that context, I recommend reading a slim volume titled Signature of Controversy, which collects responses to the critics of Meyers' magnum opus. Signature of Controversy can be downloaded for free from the website of the Discovery Institute if you subscribe to one of their free email newsletters (go to www.discoveryinstitutepress.com), or it can be ordered in conventional book form from Amazon.com. Each response in the book directs the interested reader to the Internet to find the original article or review that the response addresses.

What I hope readers of these two books will appreciate is that conflicting scientific claims can only be properly adjudicated by impartially investigating the evidence, and not by excluding an important claim because of an a priori philosophical bias, such as by incorporating the opposing claim into the definition of "science." When scientists stoop to such dogmatism to protect a cherished theory, they make the protected claim unfalsifiable, and hence unscientific.

Read the entire article here.