Science and Culture Today | Page 1205 | Discovering Design in Nature

In his next installment Professor Ussery complains that I wasn’t enthusiastic enough in my chapter “What Darwinism Can Do.” As an example of common descent I pointed to Baker’s yeast, for which there is good evidence that sometime in the past its genome duplicated. But I also noted that other yeasts with unduplicated genomes have done fine for themselves. The point was that gene or even whole genome duplication is not the powerful tool that Darwinists often claim. That point passed over Dave’s head. His main comment on the book’s next chapter, “What Darwinism Can’t Do” is to tell the reader to search PubMed for the words “cilium” and “evolution.” One gets lots of papers that contain both those words, he assures us. He naively assumes that means progress is being made on how the cilium could have arisen by a Darwinian mechanism. Ussery is simply wrong. Most of those papers have nothing to do with how the cilium evolved. Others contain interesting studies of which ciliary proteins are similar to which other proteins (which at best concerns only the topic of common descent) as well as vague, speculative scenarios, but none of the papers describes in testable detail how a structure like the cilium could have arisen step-by-step by a Darwinian mechanism. Dave’s argument might be dubbed “The Argument from Personal Credulity” — because he and others believe the cilium could arise by Darwinian means, it must have done so, and any paper that agrees it happened must contain strong evidence that it did happen. Credulity, however, is not ordinarily considered a scientific virtue.

[Editor’s Note: This is the final post in a six-part a series from microbiologist Donald L. Ewert, where he argues that the processes used by our immune system to generate antibodies are anything but “random,” and do not serve as an example of Darwinian evolution. Other posts in this rebuttal can be found at: Part One, Part Two, Part Three, and Part Four, and Part Five. In the first five posts, Dr. Ewert responded to Kathryn Applegate of the BioLogos Foundation. In this sixth post, he responds to similar arguments from Edward Max at TalkOrgins that antibody generation is “evolution in miniature.”]

One of the goals of Edwards Max’s post at TalkOrigins is to refute a narrow claim of “creationists” that “random mutations are detrimental.” But he goes further and, like Applegate, asserts that “clearly what we observe in the antibody response is evolution in miniature.” Max believes that because affinity maturation of antibodies is an established biological process, it therefore carries more weight than the computerized model of evolution used by Richard Dawkins to demonstrate that “without the intervention of any intelligent designer…successive rounds of mutation and selection could be unambiguously shown to lead to increased fitness within living organisms.” Like Applegate, Max draws inspiration from a naíve reductionist view of affinity maturation to give false comfort for his philosophical perspective.

This just in from Tom Woodward: A special edition of the weekly “Darwin or Design” program, featuring Trinity College Research Professor Tom Woodward’s interview with Discovery Senior Fellow John West, is airing tonight, Thursday, November 18th. The hour-long program begins at 7 pm Eastern (6 pm Central, 4 pm Pacific) on the Salem Network station in Tampa, WTBN, at AM 570. The discussion centers on the scientific and philosophical issues in the origins contoversy among naturalistic Darwinists, theistic evolutionists, and design theorists. Those outside Central Florida can listen live via the internet by clicking here.. The topic is the new book, God and Evolution, edited by Discovery Fellow Jay Richards. Dr. West contributed the opening chapters of the book, and Read More ›

The first part of Professor Ussery’s review of The Edge of Evolution on the website BioLogos is mainly an exercise in throat clearing, where he describes his “philosophical and personal perspective,” notes that he and I agree on common descent, and correctly points out that my book concerns the mechanism of evolution. In the second installment Dave begins to show that he somehow just doesn’t get the big points of the book. In writing of the sickle cell and other antimalarial mutations which degrade the genome, I had said that they were “hurtful.” He misunderstands this, writing, “the example [Behe] gives us is not a ‘good mutation.'” But the sickle cell and other antimalarial mutations most certainly are “good” mutations in a Darwinian sense because they are adaptive — they help the organism survive. Think of it — it was already known that most mutations that have an observable effect are deleterious. But now we know that even “good,” adaptive mutations frequently damage or break genes. That is a fact that seems to be off most Darwinists’ radar screens, although it is a profound challenge to their theory.

Dave then first employs what turns out to be a frequent tool of his: citations of papers in the literature (implying they support his position) without even an attempt to explain how they pertain to the mechanism of evolution or the edge to Darwinian evolution that I argue for in my book. He cites one paper, “Origins, evolution, and phenotypic impact of new genes,” without saying how it is known the genes arose by Darwinian processes or citing where it was that I said gene duplication and diversification couldn’t produce new genes. (I said no such thing — the book concerns the limits to Darwinian evolution; it does not say Darwinian processes can’t do anything, and I discuss the likely Darwinian origins of genes for antifreeze proteins in the chapter “What Darwinism can do.”) He cites another paper “about recent evolution of beneficial mutations in humans” without saying what those mutations are, whether they are simple or complex, or whether they are constructive or (like antimalarial mutations) degradative. A reader of Dave’s post would be quite surprised to discover that one of the last subsections of the article is called “Is Darwinian evolution enough?” where the author gingerly writes that non-Darwinian mechanisms (although — God help us — not intelligent design) “should not be categorically dismissed.” Someone just might suspect that Dave is being misleading here, but I think it much more likely that he is so enchanted by Darwinian theory that he sees overwhelming evidence for it in any paper that contains the word “evolution.”

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.

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.

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.

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.

[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.

[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 (T_H) and the interaction of Class II MHC proteins.