I explained previously the lack of details in the citations given by the NCSE (and Ken Miller, and Judge Jones) to purportedly explain the evolutionary origin of information. Their bluffs were taken from a paper by Long et al. published in Nature Reviews Genetics in 2003. More examples from that paper could be given, but the point is clear enough already: a careful analysis of Long et al. exposes the utterly insufficient explanations offered by neo-Darwinists to account for the origin of new genetic information.

In not a single case did the above papers cited by Long et al. actually explain how new functional information arose. In no case was there an analysis of how natural selection could have favored mutational changes that were shown to be likely along each step of an alleged evolutionary pathway; never was any detailed step-by-step mutational pathway even given. At best, these studies offered vague and ad hoc appeals to duplication, rearrangement, and natural selection — often in a sudden, extreme, and abrupt manner — to form the gene in question. In many cases, natural selection was invoked to allegedly account for changes in the gene, even though the investigators didn’t even know the function of the gene and thereby could not identify the advantage provided by the gene’s function. In no case were calculations performed to assess whether sufficient probabilistic resources existed to produce the asserted mutational events on a reasonable timescale. In some cases, the original genetic material for the genes was unknown, or the studies asserted spontaneous “de novo” origin of genes from previously non-coding DNA. While they readily admitted that “de novo” gene emergence is rare, no attempt was made to assess whether such an unguided mechanism is even remotely plausible on mathematical probabilistic grounds. These papers play the Gene Evolution Game, but never ask the right questions to explain how neo-Darwinian mechanisms create new genetic information.

The NCSE’s (and Judge Jones’s) citation bluffs have not explained how neo-Darwinian mechanisms produce new functional biological information. Instead, the mechanisms invoked in these papers are vague and hypothetical at best:

exons may have been “recruited” or “donated” from other genes (and in some cases from an “unknown sou[r]ce”);

there were vague appeals to “extensive refashioning of the genome”;

mutations were said to cause “fortuitous juxtaposition of suitable sequences” in a gene-promoting region that therefore “did not really ‘evolve’”;

researchers assumed “radical change in the structure” due to “rapid, adaptive evolution” and claimed that “positive selection has played an important role in the evolution” of the gene, even though function of the gene was not even known;

genes were purportedly “cobbled together from DNA of no related function (or no function at all)”;

the “creation” of new exons “from a unique noncoding genomic sequence that fortuitously evolved” was assumed, not demonstrated;

we were given alternatives that promoter regions arose from a “random genomic sequence that happens to be similar to a promoter sequence,” or that the gene arose because it was inserted by pure chance right next to a functional promoter.

explanations went little further than invoking “the chimeric fusion of two genes” based solely on sequence similarity;

when no source material is recognizable, we’re told that “genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors” because they are simply “hypermutable”;

we even saw “a striking case of convergent evolution” of “near-identical” proteins.

To reiterate, in no cases were the odds of these unlikely events taking place actually calculated. Incredibly, natural selection was repeatedly invoked in instances where the investigators did not know the function of the gene being studied and thus could not possibly have identified any known functional advantages gained through the mutations being invoked. In the case where multiple mutational steps were involved, no tests were done of the functional viability of the alleged intermediate stages. These papers offer vague stories but not viable, plausibly demonstrated explanations for the origin of new genetic information.

Within modern evolutionary biology, there are indeed many unanswered questions about how unguided selection acting upon random mutation produces new functional biological information. This will be the legacy of the Kitzmiller ruling: It pretends that fundamental scientific questions have been answered, when no adequate answers exist, at least not from the neo-Darwinian paradigm. As a result, the approach taken by Judge Jones and his consorts at the NCSE not only would miseducate students, but it threatens to hinder scientific progress by pretending that some of the most important questions in biology are answered, when they really aren’t. The myth unfortunately has become a pillar of how evolution is explained and defended in law, academia, education and the media.

Posted by Casey Luskin at 9:59 AM | Permalink | TrackBacks (0)

During the Kitzmiller v. Dover trial, Judge Jones followed Ken Miller and the NCSE by citing a review paper co-authored by Manyuan Long.⁴² Jones claimed the paper shows “peer-reviewed scientific publications showing the origin of new genetic information by evolutionary processes.”⁴³ In fact, what Long et al. actually demonstrates is that neo-Darwinists do not want to ask the right questions — the hard questions — about the sufficiency of their theory to explain gene evolution. They accept superficial just-so stories in place of detailed, plausibly demonstrated explanations.

Just as in the Gene Evolution Game, the studies cited in the review by Long et al. repeatedly invoke gene duplication, natural selection, and genetic rearrangements. But many offer little more than vague just-so stories that commit the mistakes Lynch warns of — mistaking story-telling for explanation.

To show how heavily the NCSE relies on Long et al. in its response to Explore Evolution, let’s look at how the NCSE reproduces a lengthy table (Table 2) from Long et al. The table lists a number of genes whose evolutionary origin has supposedly been explained.⁴⁴ Many of the examples from this Table 2 are mere story-telling exercises based upon assumptions which do not explain or answer deeper questions about how neo-Darwinian evolution generates new functional genetic information:

a. Jingwei
The first entry in the table comes from a study that Long co-authored with Charles Langley in Science. The study asserts that a fruit fly gene, jingwei, arose when part of another gene, Adh, was retrotransposed into a new location on a fruit fly chromosome near a duplicate of the gene yellow-emperor. ⁴⁵ Their evidence for this rearrangement is sequence similarity between part of jingwei and Adh, and part of jingwei and yellow-emperor. Thus, invoking Gene Evolution Game Rules 1 and 3, the authors tell a story that presumes that hypothetical duplicates of yellow-emperor and Adh were fortuitously spliced together to create a new functional gene—jingwei. The exact word used is that exons were “recruited” from elsewhere into the genome “by capturing several upstream exons and introns of an unrelated gene” to produce “a new functional gene.” They author make no attempt to address the more important questions, such as whether a step-wise path to such a genomic rearrangement could have happened by unguided chance to fortuitously produce this gene. Merely finding sequence similarity between exons and other genes (or pseudogenes) does not thereby demonstrate neo-Darwinian evolution.

Long et al. claim that jingwei is only 2.5 million years old, but the original study compared the Adh-like exon in jingwei with the allegedly ancestral exon from Adh and found that they were so different that they must have diverged at least 30 million years ago. This poses a problem, because this fruit fly clade is not thought to be nearly that old; as Long and Langley write, “This conflicts with the age of the melanogaster subgroup, which is estimated to be 17 to 20 million years.” More important, the unexpectedly high degree of differences between the exons is taken, under neo-Darwinian assumptions, as evidence that jingwei “responded to positive natural selection and evolved a new function.” Yet according to one commentator, despite the fact that they are sure natural selection drove this gene to acquire its new function, “its actual function is obscure.”⁴⁶ So they claim that natural selection was the driving mechanism, but they do not even know for sure in this paper that the gene has a function. They have not addressed any of the deeper questions of gene evolution, instead offering an incomplete and assumption-based story that ignores warnings from Austin Hughes against invoking “positive selection divorced from any biological mechanism.” ⁴⁷

b. Sdic
A second study cited by Table 2 asserts that various genes were duplicated, parts of which were then fused to create a new gene “de novo.”⁴⁸ The authors wanted to explain how part of one gene, Cdic, became fused with part of another gene, Annx, but they ran into problems because the genes exist on the chromosome in a different order from the gene being studied. Making complicated use of Rules 1 and 3 of the Gene Evolution Game, they speculate that there was a series of duplications and rearrangements—highly selective and specific deletions—and then more duplications to produce this gene. This included one non-coding region spontaneously becoming a coding region, termed the de novo origin of a gene. After this complicated story, the paper concludes that Sdic arose from “extensive refashioning” of the genome.

First, although a testes-specific promoter was essential for Sdic, this unusual regulatory region did not really “evolve.” Instead it was aboriginal, created de novo by the fortuitous juxtaposition of suitable sequences. The more extensive evolutionary changes took place in Cdic intron 3, enabling an originally untranslatable sequence to become a new coding region whose product functions in the assembly of axonemal dynein. ⁴⁹

This “de novo” origin of a functional gene is an event that even Long et al. admits is “rare.”⁵⁰ The authors then invoke strong positive selection due to the unlikelihood that such a dramatic reorganization “would have originated and been maintained in the absence of positive selection.” Despite their appeal to positive selection, the authors admit they aren’t even sure exactly what the gene does, stating: “We do not yet know how Sdic contributes to the function of the sperm axoneme, or even whether it is essential for male fertility.” So once again, they are sure it evolved due to “positive selection” but they do not even know exactly what function was being selected for.

A gene’s being “created de novo by the fortuitous juxtaposition of suitable sequences,” a mechanism that is “rare,” is not a compelling evolutionary explanation. This incomplete just-so story vaguely appeals to multiple mutations without assessing whether they would be likely to occur or what advantage they are offering. The story is no explanation at all.

c. Cid
The authors of this paper studied nucleotide differences between Cid genes in two closely related fruit fly species and found that nucleotide differences that led to changes in amino acid sequence were nearly 10 times more common than “silent” differences that did not affect amino acid sequence.⁵¹ Using Darwinian assumptions and Gene Evolution Game Rule 2, this led the authors to conclude that there was positive selection pressure on the gene to evolve.

Yet in this study natural selection was invoked not only to explain how genes changed, but also how genes stayed the same: a low number of replacement changes were taken as evidence of a “selective sweep,” a strong purifying selection that weeded out variation, to prevent change in one lineage. Thus, both a high degree of amino-acid changing differences and a low degree of amino-acid changing differences were taken as evidence of natural selection. Whether any of this is correct is purely a matter of ad hoc inference and starting assumptions. Moreover, the authors provided no mutation-by-mutation account to explain the selective advantages (or lack therefore) that might have been generated by any amino acid changes.

In light of the study’s methodology, Michael Lynch's warning now comes to mind. It is a “myth” to believe that “[c]haracterization of interspecific differences at the molecular and/or cellular levels is tantamount to identifying the mechanisms of evolution.” Additionally, this study violates Austin Hughes’s admonition against “the widespread use of certain poorly conceived statistical methods to test for positive selection” which have caused “the literature of evolutionary biology [to become] glutted with extravagant claims of positive selection on the basis of computational analyses alone” resulting in a “vast outpouring of pseudo-Darwinian hype [that] has been genuinely harmful to the credibility of evolutionary biology as a science.”⁵² It's also noteworthy that this study merely investigated how variations of the same gene originated in two closely related species, not how a new gene originated in the first place.

d. Arctic AFGP and Antarctic AFGP
Two papers cited by Table 2 in Long et al. discuss the origin of antifreeze genes (AFGP) in species of Arctic and Antarctic fish. The two species have similar antifreeze genes, even though they exist on literally opposite sides of the globe and are only distantly related. For the neo-Darwinist, these findings require that “near-identical antifreeze glycoproteins”⁵³ evolved independently in distantly related species of fish—one in the Arctic and another in the Antarctic—via what is called “a striking case of convergent evolution.”⁵⁴

Employing Gene Evolution Game Rules 1 and 3, a paper commenting on this research states the genes arose by “[d]uplication, divergence, and exon shuffling” and were “cobbled together from DNA of no related function (or no function at all).”⁵⁵ For key parts of the antifreeze gene in Arctic cod, the commentators noted that the investigators “did not find any database matches to the sequence”⁵⁶ and therefore could not determine its origin. However, there were matches for the Antarctic AFGP sequence, where similarities were found with part of a trypsinogen gene. This led to speculation about an evolutionary scheme that started with a trypsinogen gene, most of which was then deleted, followed by “recruitment” of a short threonine-alanine-alanine coding element, which then led to “de novo amplification of a short DNA sequence to spawn a novel protein with a new function.”⁵⁷ This “de novo amplification of the coding element gave rise to an entirely new coding region that encodes the repetitive tripeptide backbone of AFGP,” even though this key component had “arisen (in part) from noncoding DNA.”⁵⁸ Thus, according to their story, non-coding DNA spontaneously became functional and was duplicated many times to create the core functional “backbone” of this gene. No attempt was made to assess the mutational odds of such DNA that has “no function at all” suddenly becoming a key functional component of this gene.

This evolutionary story also solves problems through vague appeals to Gene Evolution Game Rule 2. The many genetic changes necessary to suddenly create this functional antifreeze gene were apparently accounted for by simply appealing to “powerful environmental selectional pressure” due to the need of the fish to survive in cold water.⁵⁹ Of course, no statistical analyses were performed to assess the likelihood of cobbling together functional genes from completely unrelated stretches of DNA, some of which was previously non-functional, to produce a new functional antifreeze gene. Rather, one paper simply asserted the “creative” power of “molecular mechanisms”:

To consider the AFGP story as a special case of duplication and divergence would be oversimplifying; it is clear that the antifreeze function, or even a related function that could be converted to the purpose, was not present in trypsinogen. The molecular mechanisms involved in the formation of this gene were indeed more creative—making sense from nonsense—by calling into a functional coding capacity intronic DNA sequences.⁶⁰

Are these molecular mechanisms likely to produce this gene? Are random mutations likely to “mak[e] sense from nonsense”? No analysis was given. The antifreeze genes are polyproteins, meaning they are complex many-in-one proteins designed to be cut into many pieces of specific lengths, each of which performs an important antifreeze function. The different segments are separated by special separator markers and cleaved by a specific protease. In this regard, no analysis was given to account for the origin of associated cleaver protease enzymes necessary for the function of the AFGP gene.

These papers base their claims of evolution purely upon circumstantial evidence—comparisons of sequence similarity—and then tell a tale of deletion, reshuffling, and amplification. Explanation of these genes by “cobbling” via “[d]uplication, divergence, and exon shuffling” and “de novo” recruitment of non-coding sequences does not account for how such a complex gene could actually originate. This story does not address how the complex many-proteins-in-one nature of these proteins evolved, nor was any consideration given the odds of spontaneously producing this functional gene. Nor have these investigators explained the highly unlikely event that two species would independently evolve highly similar antifreeze proteins.

The antifreeze proteins are highly repetitive, and may have less specified complexity than most proteins. Nonetheless, there’s no real evidence for neo-Darwinian evolution here, only sequence comparisons and a lot of missing details.

e. Adh-Finnegan
This article cited by Long et al. represents an example where a stretch of DNA that was previously presumed to be a “nonfunctional” pseudogene turned out to be a functional gene. ⁶¹ The functional gene was then named Adh-Finnegan after “Tim Finnegan, a character from an Irish folksong, [who] was mistakenly declared dead and subsequently arose during his own wake.” This is a good example of how the junk-DNA myth initially led scientists to the wrong conclusion about this gene.

This paper’s just-so story makes use of all three rules of the Gene Evolution Game. Despite its citation in Long et al. (and thus by the NCSE), the study sheds very little light on the origin of the gene in question, other than to claim it evolved from another highly similar Adh gene and then “recruited” sequences via rearrangement from elsewhere in the genome. Predictably, an ancient duplication event is invoked to account for the origin of the gene, and then selection is invoked as a magic wand to account for “radical change in the structure” of the gene “compared to that of its highly conserved Adh ancestor.”

Extensive rearrangements are also invoked to explain how the gene “recruited ~60 new N-terminal amino acids,” as well as “the acquisition of new amino acid residues upstream from the ancestral ATG initiation codon.” The origin of the N-terminal exon posed a problem, however, because “A database search revealed no similarity of the N-terminal exon to known proteins,” and thus as Long et al. note, the gene must have “[r]ecruited a peptide from an unknown souce [sic].” The author claims that a “rapid rate of evolution” of the exon prevented its identification. Thus, the paper concludes: "For the moment we will posit that a genomic rearrangement (perhaps resulting from unequal crossing over) juxtaposed the first exon from an unknown donor gene to the 5'-flanking region of the ancestor of Adh-ψ.” The mutational odds of suddenly rearranging these stretches of DNA into one place to compose a functional gene are never considered.

Ignoring the warnings of AustinHughes, the author asserted, incredibly, that there was “rapid, adaptive evolution” and that “positive selection has played an important role in the evolution” of this gene even though the function of the gene is not known.

f. FOXP2
This gene is commonly cited as being involved in the origin of human language, even though it’s not exactly clear what it does. ⁶² In fact, one study observed that “The finding that FOXP2 is critical to speech and language does not by itself demonstrate the role of this gene in the origin of human speech, because the function of FOXP2 could have remained unchanged during human evolution while other speech-related genes changed.”⁶³

The studies cited by Long et al. compared human FOXP2 to copies of the same gene in chimps, gorillas, orangutans, the macaque, and mice, and found that “FOXP2 is a conserved protein, with only three amino acid differences (and a 1-amino-acid insertion/deletion) between human and mouse in its entire length of 715 amino acids.”⁶⁴ Thus, this paper did not really study the origin of a new gene, but only tried to explain how human FOXP2 obtained a mere two differences in amino acid sequence from FOXP2 in apes.

In this case, the high ratio of non-synonymous (i.e. amino acid changing) to synonymous (i.e. silent) nucleotide differences was taken as evidence of the force of “positive selection.” ⁶⁵ Again, selection is being inferred, even though the authors didn’t know exactly what the gene does, violating Austin Hughes’s warning against “statistically based claim[s] of evidence for positive selection divorced from any biological mechanism.”⁶⁶ At base, these studies catalogued interspecific differences between human FOXP2 and FOXP2 from other species, and found that those differences were extremely slight. Even if neo-Darwinian mechanisms were indeed at work, the degree of evolution in human FOXP2 amounts to 2 mutations, and 2 amino acid changes. This is an interesting finding, but not useful in explaining any actually noteworthy or impressive degrees of genetic evolution.

g. Cytochrome c1
This paper sought to explain the origin of a gene, cytochrome c1, involved in energy production in plants.⁶⁷ The study found sequence similarity between three exons in cytochrome c1, a gene that operates in the mitochondria, with a gene with a very different function, GapC, which operates in the cytoplasm.⁶⁸ That sequence similarity, essentially, formed the entire basis for this evolutionary story of rearrangement of exons, which made heavy use of Gene Evolution Game Rule 3. Since cytochrome c1 is less widespread than Gapc1, the authors concluded that Gapc1 is older and therefore “donated” the exons to cytochrome c1 through “exon shuffling.” Additionally, they speculate that the ancestral cytochrome c1 gene had the same function, but these new exons (for some reason) allowed the same function to be performed—but even more efficiently: “The ancestral cytochrome c1 gene in plants must have been targeted to the mitochondrion; thus this targeting sequence was replaced in the line leading to the potato by the GapC gene. This replacement may have been selected by some advantage in using the GapC promoter.” Predictably, the authors never discuss the mutational odds of replacing exons in one gene with exons “donated” from another gene such that the gene not only remains functional but has an advantage in performing its original function. This is the key phase where new genetic information must arise, but the authors never assess whether it would be likely to occur via unguided mutations.

h. Morpheus
This study aimed to explain the origin of a group of genes named morpheus that had changed so much that their origin could not be traced to any other gene. As the paper lamented, “some genes emerge and evolve very rapidly, generating copies that bear little similarity to their ancestral precursors” and thus “may not possess discernable orthologues within the genomes of model organisms.”⁶⁹ When studying these genes, they reported “no significant sequence similarity to this gene family in other organisms at either the nucleotide or protein level.” Since it was impossible to invoke a scheme of duplications or other rearrangements from which this genetic material found its origin, the authors simply concluded, “These data suggested that the exonic regions were hypermutable or that amino-acid changes had been selected during the evolution of this gene family” and that their “analysis has revealed an extraordinary degree of evolutionary plasticity.” In other words, they have no idea where this gene came from, so they invoke the claim that the genes were “hypermutable” and subject to strong selection pressure such that their origin cannot be traced. How the genes actually arose is a question the authors never really address. Incredibly, they again appeal to strong selection pressure despite admitting “the precise function of this gene family is unknown.” Gene Evolution Game Rule 2 solved all the problems without anyone’s having to investigate the plausibility of the mechanism.

i. TRE2
This paper invoked “the chimeric fusion of two genes” to explain how the gene Tre2 evolved from duplicates of two other genes.⁷⁰ The story is simple: Tre2 has 30 exons: exons 1-14 appear similar to another gene, TBCID3, while exons 15-30 are similar to the gene USP32. Thus the authors characterized the origin of this gene as “the abrupt creation of a mosaic gene with novel functions.” Although the authors claim that “domain accretion and gene-fusion events may not be uncommon,” they offered no consideration of the odds of mutations rearranging these two genes in a fashion that is functional and performs some new and useful function.

j. Dntf-2r
This study, co-authored by Long, claimed that Dntf-2r, a fruit fly gene, arose as a duplicate that was retrotransposed from the gene Dntf-2. Using Gene Evolution Game Rule 2, the authors attempt to explain the subsequent evolution of Dntf-2r by assessing the ratio of non-synonymous to synonymous differences. Using one test, they found that “polymorphism is higher for synonymous than for replacement sites ... revealing the action of purifying selection,” however another test “revealed a significant excess of amino acid substitutions, suggesting that the accelerated protein sequence evolution is likely a consequence of the action of positive Darwinian selection.” To explain these seemingly contrary results, they decided that “both purifying selection and adaptive evolution” were at work. But they did not try to explain exactly what functions these forces were working to preserve or to change because the authors didn’t know the function of Dntf-2r. Before their study “there was no information on the function of Dntf-2r” and after their study, all they could say was “this gene may produce a functional protein.” Once again, positive selection is being conjured even though it is “divorced from any biological mechanism.”⁷¹ One would certainly like to know the mutational pathway taken or the selective advantage offered by specific mutations along that pathway. None of this is discussed, meaning an explanation for the evolution of new genetic information is absent from this paper.

The authors also tried to explain the origin of the promoter for Dntf-2r, rightly noting that “Whether or not a retroposed sequence recruits a new promoter is a critical step to its future fate. If a retroposed sequence integrates in a genomic region devoid of expression potential, it would be doomed to evolve into a pseudogene.” So how did Dntf-2r get its promoter? The authors found that Dntf-2r’s promoter fortuitously comes from DNA near where it’s located (its insertion site), but state that “it is unclear if this previously existing sequence is a functional promoter for some unknown gene in the region or is just a random genomic sequence that happens to be similar to a promoter sequence.”⁷² The authors make no attempt to assess the plausibility of these alternatives: they assess neither the likelihood of a “random genomic sequence” suddenly becoming a functional promoter sequence, nor the likelihood of a gene being inserted by chance right next to a functional promoter.

k. Sanguinaria rps1
This paper was inspired by the finding of “three striking distributional anomalies in a survey of mitochondrial gene content in angiosperms.”⁷³ In other words, they found genes in species where they weren’t expected under the conventional understanding of common descent, because the same genes were found in supposedly “distantly related flowering plants.” Following Ragan and Beiko (“topological discordance between a gene tree and a trusted reference tree is taken as a prima facie instance of LGT [lateral gene transfer]”⁷⁴), the authors assume that this phylogenetic incongruity is the result of LGT. This paper thus did not really explain the actual origin of these genes, but simply assumed and asserted that wherever and however they evolved, the genes were transplanted into these flowering plants via LGT (also known as horizontal gene transfer, or “HGT”).

The authors conclude that these data “establish for the first time that conventional genes are subject to evolutionarily frequent HGT during plant evolution and provide the first unambiguous evidence that plants can donate DNA horizontally to other plants.” Yet the authors admitted that the question “How do genes move from one plant to another, sexually unrelated, plant?” remains unanswered. Thus, evidence for HGT in plants is based merely upon the incongruent distribution of these genes assuming the standard phylogeny, not any actually established mechanism of HGT in flowering plants. Indeed, the authors admit that “horizontal transfer is unknown within the evolution of animals, plants and fungi except in the special context of mobile genetic elements.” This paper thus tells us virtually nothing about the actual original evolutionary birth of these genes, wherever they first originated, and instead highlights the assumptions and ad hoc reasoning used to save common descent from falsification by contrary phylogenetic data.

While studying this gene in various plant species, the authors found two additional instances of HGT, one of which was in Sanguinaria canadensis (bloodroot), a dicot whose rps11 gene “turns out to be chimaeric: its 5’ half is of expected eudicot, vertical origin, but its 3’ half is indisputably of monocot, horizontal origin.” In other words, half the gene appears like dicot rps11 and the other half appears like monocot rps11, and it is therefore identified as “chimaeric.” According to this story, monocot rps11 was transported into the Sanguinaria genome (by an unknown mechanism) and then, just by chance, happened to fuse with the dicot version of the same gene to create a new functional gene. The authors never discuss whether it is remotely plausible to claim that a gene would be transported from another species (by an unknown mechanism) only to fuse with its own homologue in the new genome—just by chance—and then create a new functional gene.

l. PMCHL
Despite the NCSE’s smooth assurance that “Biologists have no trouble showing how new information (in the sense used by information theorists) originates, nor how new genes, kinds of cells or tissues evolve,” this 2001 paper opens by admitting that “How genes with newly characterized functions originate remains a fundamental question.” ⁷⁵ Like the Sdic and AFGP examples, the origin of PMCHL1 and PMCHL2, considered here, required the “de novo” creation of key components of the gene where an exon “originated from a unique noncoding sequence.” The authors describe this process as requiring the “creation of 3’ exons from a unique noncoding genomic sequence that fortuitously evolved as a standard intron-exon structure and polyadenylation signal sequences.” Key portions of this gene therefore just “fortuitously evolved.” Is that an explanation? The paper does not want to encourage such arbitrary explanations, and thus the authors caution that “de novo generation of building blocks—single genes or gene segments coding for protein domains— seems to be rare.”

Accounting for the origin of the rest of this gene proved extremely complicated, but Gene Evolution Game Rules 1 and 3 allowed the authors to invoke a series of rearrangements including retrotranspositions, insertions, and duplications. They propose that these genes were suddenly “co-opted” or “‘exapted’ into a functional role.” While the origin of genes with new functions is indeed a “fundamental question,” this paper’s reliance on “fortuitously evolved” explanations does very little to answer that question. This is especially true considering that the authors offered no analysis of the mutational odds of converting noncoding DNA to coding DNA and recruiting and rearranging multiple segments of the genome to create a new functional gene.

References Cited:

[42.] Manyuan Long, Esther Betrán, Kevin Thornton, and Wen Wang, “The Origin of New Genes: Glimpses from the Young and Old,” Nature Reviews Genetics, Vol. 4:865-875 (November, 2003).

[43.] Kitzmiller v. Dover, 400 F.Supp.2d 707, 744 (M.D.Pa. 2005).

[44.] See Limits on Evolution at http://ncseweb.org/creationism/analysis/extrapolations

[45.] Manyuan Long & Charles H. Langley, “Natural selection and the origin of jingwei, a chimeric processed functional gene in Drosophila,” Science, Vol. 260:91–95 (April 2, 1993).

[46.] John M. Logsdon, Jr., & W. Ford Doolittle, “Origin of antifreeze protein genes: A cool tale in molecular evolution,” Proceedings of the National Academy of Sciences USA, Vol. 94:3485-3487 (April, 1997).

[47.] Austin L. Hughes, "Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level," Heredity, Vol. 99:364–373 (2007).

[48.] Dmitry I. Nurminsky, Maria V. Nurminskaya, Daniel De Aguiar, and Daniel L. Hartl, “Selective sweep of a newly evolved sperm-specic gene in Drosophila,” Nature, Vol. 396:572-575 (December 10, 1998).

[49.] Id.

[50.] Manyuan Long, Esther Betrán, Kevin Thornton, and Wen Wang, “The Origin of New Genes: Glimpses from the Young and Old,” Nature Reviews Genetics, Vol. 4:865-875 (November, 2003).

[51.] Harmit S. Malik and Steven Henikoff, “Adaptive Evolution of Cid, a Centromere-Specific Histone in Drosophila,” Genetics, Vol. 157:1293–1298 (March 2001).

[52.] Austin L. Hughes, "The origin of adaptive phenotypes," Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193–13194 (Sept. 9, 2008) (internal citations removed).

[53.] Liangbiao Chen, Arthur L. DeVries, & Chi-Hing C. Cheng, “Convergent evolution of antifreeze glycoproteins in Antarctic notothenioid fish and Arctic cod,” Proceedings of the National Academy of Sciences USA, Vol. 94:3817–3822 (April, 1997).

[54.] John M. Logsdon, Jr., & W. Ford Doolittle, “Origin of antifreeze protein genes: A cool tale in molecular evolution,” Proceedings of the National Academy of Sciences USA, Vol. 94:3485-3487 (April, 1997).

[55.] Id.

[56.] Id.

[57.] Liangbiao Chen, Arthur L. DeVries, & Chi-Hing C. Cheng, “Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish,” Proceedings of the National Academy of Sciences USA, Vol. 94:3811–3816 (April, 1997).

[58.] John M. Logsdon, Jr., & W. Ford Doolittle, “Origin of antifreeze protein genes: A cool tale in molecular evolution,” Proceedings of the National Academy of Sciences USA, Vol. 94:3485-3487 (April, 1997).

[59.] Liangbiao Chen, Arthur L. DeVries, & Chi-Hing C. Cheng, “Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish,” Proceedings of the National Academy of Sciences USA, Vol. 94:3811–3816 (April, 1997).

[60.] John M. Logsdon, Jr., & W. Ford Doolittle, “Origin of antifreeze protein genes: A cool tale in molecular evolution,” Proceedings of the National Academy of Sciences USA, Vol. 94:3485-3487 (April, 1997).

[61.] David J. Begun, “Origin and Evolution of a New Gene Descended From alcohol dehydrogenase in Drosophila,” Genetics, Vol. 145:375-382 (February, 1997).

[62.] Wolfgang Enard, Molly Przeworski, Simon E. Fisher, Cecilia S. L. Lai, Victor Wiebe, Takashi Kitano, Anthony P. Monaco & Svante Pääbo, “Molecular evolution of FOXP2, a gene involved in speech and language,” Nature, Vol. 418:869-872 (August 22, 2002) (stating “to establish whether FOXP2 is indeed involved in basic aspects of human culture, the normal functions of both the human and the chimpanzee FOXP2 proteins need to be clarified”).

[63.] Jianzhi Zhang, David M. Webb and Ondrej Podlaha, “Accelerated Protein Evolution and Origins of Human-Specific Features: FOXP2 as an Example,” Genetics, Vol. 162:1825–1835 (December 2002).

[64.] Id.

[65.] Id.

[66.] Austin L. Hughes, "Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level," Heredity, Vol. 99:364–373 (2007).

[67.] Manyuan Long, Sandro J. de Souza, Carl Rosenberg, and Walter Gilbert, “Exon shuffling and the origin of the mitochondrial targeting function in plant cytochrome cl precursor,” Proceedings of the National Academy of Sciences USA, Vol. 93:7727-7731 (July, 1996).

[68.] Id. Specifically, the authors write: “In a computer survey of an exon database, we observed a high similarity (44% identity and 64% similarity over 41 amino acids) between the 5’ three consecutive exons of the pea Gapc1 and the potato cytochrome c1 precursor.”

[69.] Matthew E. Johnson, Luigi Viggiano, Jeffrey A. Bailey, Munah Abdul-Rauf, Graham Goodwin, Mariano Rocchi & Evan E. Eichler, “Positive selection of a gene family during the emergence of humans and African apes,” Nature, Vol. 413:514-519 (October 4, 2001).

[70.] Charles A. Paulding, Maryellen Ruvolo, and Daniel A. Haber, “The Tre2 (USP6) oncogene is a hominoid-specific gene,” Proceedings of the National Academy of Sciences USA, Vol. 100(5):2507–2511 (March 4, 2003).

[71.] Austin L. Hughes, "Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level," Heredity, Vol. 99:364–373 (2007).

[72.] Esther Betran and Manyuan Long, "Dntf-2r, a Young Drosophila Retroposed Gene With Specific Male Expression Under Positive Darwinian Selection," Genetics, Vol. 164:977–988 ( July 2003).

[73.] Ulfar Bergthorsson, Keith L. Adams, Brendan Thomason, and Jeffrey D. Palmer, "Widespread horizontal transfer of mitochondrial genes in flowering plants," Nature, Vol. 424:197-201 (July 10, 2003).

[74.] Mark A. Ragan and Robert G. Beiko, "Lateral genetic transfer: open issues," Philosophical Transactions of the Royal Society B, Vol. 364:2241-2251 (2009).

[75.] Anouk Courseaux and Jean-Louis Nahon, “Birth of Two Chimeric Genes in the Hominidae Lineage,” Science, Vol. 291:1293-1297 (February 16, 2001).

Posted by Casey Luskin at 10:00 AM | Permalink | TrackBacks (0)

As we've seen, it’s easy to duplicate a gene, but the key missing ingredient in many neo-Darwinian explanations of the origin of new genetic information is how a gene duplicate then acquires some new optimized function. Evolutionists have not demonstrated, except in rare cases, that step-wise paths to new function for duplicate genes exist.

As we saw in an earlier post, Austin Hughes cautions against making “statistically based claim[s] of evidence for positive selection divorced from any biological mechanism.”²⁶ In other words, natural selection is invoked to explain the evolution of genes where we do not even know the functional effect of the mutations being asserted. In this regard, Hughes observes that even in one of the more sophisticated studies, “there was no direct evidence that natural selection was actually involved in fixing adaptive changes.”²⁷

Hughes also acknowledges a problem inherent in many appeals to natural selection, namely that required mutations may not give any selective advantage when they first arise. He thus writes regarding one study:

For example, a rhodopsin from the Japanese conger eel with λ_max ≈ 480 nm achieved this sensitivity through the interaction of three different amino acid replacements (at sites 195, 195, and 292). There does not seem to be any way that natural selection could favor an amino acid replacement that would be of adaptive value only if two other replacements were to occur as well.²⁸

In this case, there was no stepwise advantage gained with each successive mutation. Because no advantage could have been gained until all three mutations were present, Hughes finds it more “plausible” to believe that the first two mutations were “selectively neutral” and became fixed due to random, non-adaptive processes such as genetic drift. Once the third mutation arose it might have provided an advantage, but to paraphrase Scott Gilbert, at best this really only explains the survival of the fittest, not the arrival of the fittest.²⁹

But Hughes’ explanation has deep deficiencies: it requires that two mutations become fixed before any selective advantage for the third mutation is gained. This implies that there must be three specific mutations to gain any selective advantage. A key question is thus, Are multiple specific mutational changes likely to appear in the same individual through unguided chance mutations given known mutation rates and population sizes? Even Hughes, despite his exhortations to fellow evolutionary biologists to employ more rigor in their studies, does not address this fundamental question.

A similar example is found when leading paleoanthropologist Bernard Wood critiqued a simplistic model of human cranial evolution on the grounds that too many mutations would be required to gain any functional advantage:

The mutation would have reduced the Darwinian fitness of those individuals. . . . It only would’ve become fixed if it coincided with mutations that reduced tooth size, jaw size and increased brain size. What are the chances of that? ³⁰

Similarly, Jerry Coyne writes that “It is indeed true that natural selection cannot build any feature in which intermediate steps do not confer a net benefit on the organism.”³¹ This highlights a key deficiency in many neo-Darwinian accounts of the evolution of genes. Namely, they fail to demonstrate that the processes necessary to generate new functionally advantageous genetic information are plausible. As with Hughes’s or Wood’s examples above, multiple mutations might be necessary to gain any functional advantage. Any account invoking blind, unguided, random mutations to evolve a gene from Function A to Function B must address at least these three questions:

Question 1: Is there a step-wise adaptive pathway to mutate from A to B, with a selective advantage gained at each small step of the pathway?

Question 2: If not, are multiple specific mutations ever necessary to gain or improve function?

Question 3: If so, are such multi-mutation events likely to occur given the available probabilistic resources?

Mathematician David Berlinski considers such questions when critiquing evolutionary accounts of eye evolution. Darwinian processes fail because multiple changes are required for a new function to appear:

If these changes come about simultaneously, it makes no sense to talk of a gradual ascent of Mount Improbable. If they do not come about simultaneously, it is not clear why they should come about at all. ³²

Again, the key question is therefore, how hard is it for new functional biological information to arise? Answering this question requires assessing the ability of random mutation and natural selection to generate new functional biological information. But when most evolutionary biologists play the Gene Evolution Game, they do not make such assessments and rarely consider these questions. Instead they typically invoke processes such as gene duplication, natural selection, and rearrangement, without demonstrating that random and unguided mutations are sufficient to produce the information needed. Any explanation that at base is little more complicated than “duplication, rearrangement, and natural selection” is not a demonstration that new functional genes can arise by unguided processes.

Thankfully, some scientists are willing to consider these key questions. They have performed research providing data that offers strong reasons to be skeptical of the ability of mutation and selection to form new functional genetic sequences.

A. Asking Questions 1 and 2:
Molecular biologist Doug Axe has performed mutational sensitivity tests on enzymes and found that functional protein folds may be as rare as 1 in 1077.³³ His research shows that the fitness landscape for many enzymes looks like this, making it very unlikely that neo-Darwinian processes will find the specific amino acid sequences that yield functional protein folds:


To put the matter in perspective, these results indicate that the odds of Darwinian processes generating a functional protein fold are less than the odds of someone closing his eyes and firing an arrow into the Milky Way galaxy, and hitting one pre-selected atom.³⁴ To say the least, this exhausts the probabilistic resources available. Such data help us answer the first question: it’s not likely that there will be a functional stepwise mutational pathway leading from Function A to Function B.

Douglas Axe is by no means the only biologist to make this observation. A leading college-level biology textbook, Campbell’s Biology, observes that “Even a slight change in primary structure can affect a protein’s conformation and ability to function.”³⁵ Likewise, David S. Goodsell, an evolutionist biologist, writes:

As you might imagine, only a small fraction of the possible combinations of amino acids will fold spontaneously into a stable structure. If you make a protein with a random sequence of amino acids, chances are that it will only form a gooey tangle when placed in water. Cells have perfected the sequences of amino acids over many years of evolutionary selection…³⁶

What Goodsell does not mention is that if “perfected” amino acid sequences and functional protein folds are rare and slight changes can disrupt function, then selection will be highly unlikely to take proteins from one functional fold to the next without traversing some non-functional stage. So how do new functional protein folds evolve? This effectively answers question two, implying that many specific mutations would be necessary for evolving genes to pass through non-functional stages while evolving some new function. Question 3 assesses whether this is likely to happen.

B. Asking Question 3:
In 2004, Michael Behe and physicist David Snoke published a paper in the journal Protein Science reporting results of computer simulations and theoretical calculations. They showed that the Darwinian evolution of a simple functional bond between two proteins would be highly unlikely to occur in populations of multicellular organisms. The reason, simply put, is because too many amino acids would have to be fixed by non-adaptive mutations before gaining any functional binding interaction. They found:

The fact that very large population sizes—109 or greater—are required to build even a minimal [multi-residue] feature requiring two nucleotide alterations within 108 generations by the processes described in our model, and that enormous population sizes are required for more complex features or shorter times, seems to indicate that the mechanism of gene duplication and point mutation alone would be ineffective, at least for multicellular diploid species, because few multicellular species reach the required population sizes. ³⁷

According to this data, chance mutations are unlikely to produce even two required non-adaptive mutations in multicellular diploid species within any reasonable timescale. This answers the third question: getting multiple specific non-adaptive mutations in one individual is extremely difficult, and more than two required but non-adaptive mutations are likely beyond the reach of multi-cellular organisms. Studies like this show that the actual ability of random mutation and unguided selection to produce even modestly complex new genetic functions is insufficient.

In 2008, Behe and Snoke’s would-be critics tried to refute them in the journal Genetics, but found that to obtain only two specific mutations via Darwinian evolution “for humans with a much smaller effective population size, this type of change would take > 100 million years.” The critics admitted this was “very unlikely to occur on a reasonable timescale.” ³⁸ In other words, there is too much complex and specified information in many proteins and enzymes to be generated in humans by Darwinian processes on a reasonable evolutionary timescale.

As noted in the comments on the Gene Evolution Game, when neo-Darwinists try to explain the evolution of genes, mere point mutations often are insufficient to account for the gene’s sequence. They must therefore appeal to genetic rearrangements such as insertions, deletions, or an alleged process called “domain shuffling” where segments of proteins become shuffled to new positions in the genome. In his book The Edge of Evolution, Michael Behe reviews research that engineered new protein function by swapping domains to change protein function, and found that the intelligently engineered changes required multiple modifications that, in nature, would require too many simultaneous mutational events to yield functional changes:

[Protein engineering research] does not mimic random mutation. It is the exact opposite of random mutation. ... What do the lab results tell us about whether random-yet-productive shuffling of domains “occurs with significant frequency under conditions that are likely to occur in nature”? About whether that is biologically reasonable? Nothing at all. When a scientist intentionally arranges fragments of genes in order to maximize the chances of their interacting productively, he has left Darwin far, far behind. ... [Experiments that engineered proteins by shuffling domains] didn't just splice two genes together in a single step; they took several additional steps as well. … Remember the more steps that have to occur between beneficial states, the much less plausible are Darwinian explanations. ... Domain shuffling would be an instance of the “natural genetic engineering” championed by James Shapiro where evolution by big random changes is hoped to do what evolution by small random changes can't. But random is random. No matter if a monkey is rearranging single letters or whole chapters, incoherence plagues every step. ... One step might luckily be helpful on occasion, maybe rarely a second step might build on it. But Darwinian processes in particular and unintelligent ones in general don't build coherent systems. So it is biologically most reasonable to conclude that, like multiple brand new protein-protein binding sites, the arrangement of multiple genetic elements into sophisticated logic circuits similar to those of computers is also well beyond the edge of Darwinian evolution. ³⁹

As Behe observes, “No matter if a monkey is rearranging single letters or whole chapters, incoherence plagues every step.” Thus, when multiple mutational events—whether point mutations, “domain shuffling,” or other types of rearrangements—are required to gain some functional advantage, it seems unlikely that blind neo-Darwinian processes can produce the new biological function.

Unfortunately, few if any advocates of the neo-Darwinian just-so stories investigate whether mutation and natural selection are sufficient to produce new functional genetic information. Instead they believe that finding similarities and differences between genes demonstrates that neo-Darwinian evolution has occurred, and they assume that “positive selection” is a sufficient explanation.

As Hughes cautions, they engage in “use of certain poorly conceived statistical methods to test for positive selection,” causing “the literature of evolutionary biology [to become] glutted with extravagant claims of positive selection” resulting in a “vast outpouring of pseudo-Darwinian hype [that] has been genuinely harmful to the credibility of evolutionary biology as a science.” ⁴⁰ Or, as Michael Behe cautions, they confuse mere sequence similarity with evidence of neo-Darwinian evolution. Finally, Michael Lynch warns his colleagues that “Evolutionary biology is not a story-telling exercise, and the goal of population genetics is not to be inspiring, but to be explanatory.” ⁴¹

With these principles in mind, in the next installment we will assess about a dozen of the just-so stories concerning the origin of genes offered in studies cited by the NCSE.

References Cited:

[26.] Austin L. Hughes, "Looking for Darwin in all the wrong places: the misguided quest for positive selection at the nucleotide sequence level," Heredity, Vol. 99:364–373 (2007).

[27.] Id.

[28.] Id.

[29.] “The modern synthesis is good at modeling the survival of the fittest, but not the arrival of the fittest.” Scott Gilbert, quoted in John Whitfield, “Biological Theory: Postmodern evolution?,” Nature, Vol. 455:281-284 (2008).

[30.] Bernard Wood, quoted in Joseph B. Verrengia, “Gene Mutation Said Linked to Evolution,” Associated Press, found in San Diego Union Tribune, March 24, 2004.

[31.] Jerry Coyne, "The Great Mutator," The New Republic (June 14, 2007). Coyne asserts he knows of no example where this is the case.

[32.] David Berlinski, “Keeping an Eye on Evolution: Richard Dawkins, a relentless Darwinian spear carrier, trips over Mount Improbable. Review of Climbing Mount Improbable by Richard Dawkins (W. H. Norton & Company, Inc. 1996),” in The Globe & Mail (November 2, 1996) at http://www.discovery.org/a/132

[33.] Douglas A. Axe, “Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds,” Journal of Molecular Biology, Vol. 341: 1295-1315 (2004); Douglas A. Axe, “Extreme Functional Sensitivity to Conservative Amino Acid Changes on Enzyme Exteriors,” Journal of Molecular Biology, Vol. 301: 585-595 (2000).

[34.] See Stephen C. Meyer, Signature in the Cell: DNA and the Evidence for Intelligent Design, pg. 211 (Harper One, 2009).

[35.] Neil A. Campbell and Jane B. Reece, Biology, pg. 84 (7th ed, 2005).

[36.] David S. Goodsell, The Machinery of Life, pg. 17, 19 (2nd ed, Springer, 2009).

[37.] Michael J. Behe & David W. Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” Protein Science, Vol 13:2651-2664 (2004).

[38.] Rick Durrett and Deena Schmidt, “Waiting for Two Mutations: With Applications to Regulatory Sequence Evolution and the Limits of Darwinian Evolution,” Genetics, Vol. 180: 1501–1509 (November 2008).

[39.] Michael Behe, The Edge of Evolution: The Search for the Limits of Darwinism, Appendix D, pgs. 272-275 (Free Press, 2007) (emphasis added).

[40.] Austin L. Hughes, "The origin of adaptive phenotypes," Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193–13194 (Sept. 9, 2008) (internal citations removed).

[41.] Michael Lynch, “The frailty of adaptive hypotheses for the origins of organismal complexity,” Proceedings of the National Academy of Sciences, Vol. 104:8597–8604 (May 15, 2007).

Posted by Casey Luskin at 9:04 AM | Permalink | TrackBacks (1)

Jerry Fodor and Massimo Piattelli-Palmarini aren't making many friends among evolutionists with their new book What Darwin Got Wrong. Salon magazine published an interview with Fodor today in which he has some interesting things to say about the attacks he's received online, about whether he is providing aid and succor to the ID community, and what he thinks is wrong with modern evolutionary theory.

As you explain in the book, one of the problems with Darwinism is that Darwin is inventing explanations for something that happened long ago, over a long period of time. Isn’t that similar to creationism?

Creationism isn't the only doctrine that’s heavily into post-hoc explanation. Darwinism is too. If a creature develops the capacity to spin a web, you could tell a story of why spinning a web was good in the context of evolution. That is why you should be as suspicious of Darwinism as of creationism. They have spurious consequence in common. And that should be enough to make you worry about either account.

Posted by Robert Crowther at 8:21 AM | Permalink | TrackBacks (0)

The Gene Evolution Game is a very simple game to play. In three examples, we’ll develop three rules that can help you explain the origin of any new gene. That’s right—any gene! Let’s start with a simple example:

Rule 1: The Magic Wand of Gene Duplication
Where do new genes come from? Gene duplication is typically how we explain where a new gene comes from. Here’s how it works:

(1) Take a gene you’ve observed in some organism. We’ll call it Gene B.

(2) Find another gene similar to Gene B. Let’s call it Gene A.

(3) Claim that at some time in the past, Gene A duplicated so then there were two copies of Gene A.

(4) Then assert that one of Gene A’s duplicates evolved into Gene B.

Gene duplication is thus very a powerful explanation, and it looks like this:

Wasn’t that easy? We’ve just explained how Gene B evolved! So when you find two genes with high sequence similarity, you can always explain how one evolved from the other via the magic wand of Gene Duplication.

Rule 2: No Worries—Natural Selection Can Do It!
Now obviously the modern version of Gene B we find doesn’t perfectly resemble Gene A, or else it would be Gene A. So we have to account for how a copy of Gene A acquired its new function—Function B. One might think this would be the key part of explaining how new functional genetic information arises, but believe it or not, this is actually the easiest and quickest aspect of the game: we just call upon the power of “natural selection” and the problem is solved! This diagram shows exactly how we do it:

The great thing about the Gene Evolution Game is that natural selection can change (or not change, depending on what you wish) almost anything. And I mean anything.

Don’t worry about the details. If you want to account for differences between Gene B and Gene A, natural selection is always up to the challenge. Don’t worry about whether Gene A’ could evolve from Function A to Function B by small sequential adaptive steps. Don’t worry about the order in which amino acids changed, or whether many mutations were necessary to gain any functional advantage (that sort of thing is too unlikely to occur anyway, so just ignore it). Don’t worry about adaptive constraints, weak selection, or loss due to genetic drift. And most of all, definitely don’t do any calculations to determine the likelihood of whether all of the changes could have occurred in any reasonable amount of time.

We know the gene must have evolved, therefore it did evolve. Thus, you can think of natural selection as another magic wand. It may be invoked at any time to explain how a gene changed or evolved to acquire its new function.

This wand is a very powerful tool—it can explain both why things change, and why things stay the same.²³ Wow!

Rule 3: The Magic Wand of “Rearrangement”

To play the Gene Evolution Game, there’s one last trick you need to know. Sometimes Gene B isn’t similar to just Gene A. Sometimes part of Gene B looks like Gene A, but another part looks like another gene. We’ll call the latter Gene Z. Don’t worry—this is all still easy to explain! We start by invoking duplication: Imagine that Gene A and Gene Z both duplicated, and then both duplicate copies were suddenly transported across the genome so that now they reside on a chromosome right next to one another. This is called “rearrangement.” If this sounds a little complicated, we’ll draw some diagrams to show how it works:

Step 1: Gene A and Gene Z are each in different locations, maybe even on different chromosomes:

Then a special process called “rearrangement” suddenly rearranges and transports Gene A and Gene Z so they’re right next to each other in some other location in the genome. Rearrangement is a powerful magic wand you can invoke to explain how two stretches of DNA that initially are far apart suddenly end up near one another. They then can form a new functional gene. You’re probably getting a feel by now for how this works:

There are all kinds of rearrangements you can invoke—insertions, deletions, inversions, translocations—and you can invoke them in virtually any order and in any amount you please to explain how you get any two, or three, or even dozens of pieces of DNA to come together from throughout the genome to end up right next to one-another so that presto, you have your new functional gene. Just mix and match these types of rearrangements as needed to create virtually whatever DNA sequence you desire—rearrangement is always up to the task.

It’s all downhill from here. Natural selection can then perfect the rearranged gene to make it functional. Never mind detailed demonstrations that this actually works. Just sprinkle some natural selection and Gene A and Gene Z will magically combine functions and evolve into Gene B. Here we go, completing the explanation with everything we need to know:

Using the three magic wands of duplication, rearrangement, and natural selection you can provide a full and complete detailed explanation for the evolution of virtually any gene.

No Identifiable Ancestor? No Worries!
First, in some cases, your gene (i.e., Gene B) only has a homologue known from an entirely different species. So how did Gene B arrive in your organism? In these cases, just invoke lateral gene transfer (LGT) to whoosh the right gene into your organism. It doesn’t even matter whether lateral gene transfer is thought to occur between the organisms you’re working with—if the gene you need is found in some other species, then that by itself is evidence that lateral gene transfer occurs between the organisms you’re working with!²⁴

Second, sometimes part of your gene doesn’t resemble part of any other known gene anywhere. Some people might wonder, “Where did this gene come from?” You still don’t worry about this. Remember what we said about natural selection? It can change anything. So if you can’t find any similar genes, just assume that your unique DNA sequence has evolved so much due to natural selection that it just doesn’t resemble its ancestral sequence any longer. But don’t worry, it’s not, and never is, the case that there wasn’t an ancestor. It’s just that the strong powers of natural selection changed the gene so much that we can’t identify any possible ancestral sequence.²⁵

Some Final “Do’s” and “Don’ts” of the Gene Evolution Game
Right about now, you might be wondering about that last example we gave. So before you go any further, here’s a reminder of some questions you don’t need to ask:

Given the known effects and rates of mutations, what were the odds of Gene A and Gene Z suddenly being rearranged next to one-another so that they could now function together as one single new gene product, Gene B?

Did the rearranged gene product B start out functional? If not, how quickly could it gain function? How was it preserved from loss until it became functional?

Are proteins really as malleable as this story would suppose or would the new combined gene encounter folding or other contextual problems?

What mutational pathway was taken to evolve Gene A and Gene Z into a new gene with function B?

What selective advantages were gained at each small step of this evolutionary pathway?

Were any “large steps” (i.e., multiple specific mutations) ever required to gain a selective advantage along the evolutionary pathway? Would such “large steps” be likely to occur?

Could all of this happen on a reasonable timescale?

You don’t need to worry about these questions. In fact, believe it or not, you don’t even need to know the function of your gene to claim it evolved from A and Z! All you need to know is that Genes A, Z, and B exist. This summary of these 3 simple rules of the Gene Evolution Game will help you explain anything:

Gene Evolution Game Rule 1: Whenever you find sequence homology between two genes, just invoke a duplication event of some hypothetical, ancient ancestral gene, and you can explain how two different genes came to share their similarities.

Gene Evolution Game Rule 2: When you need to explain how a gene acquired some new function, or evolved differences from another gene, just invoke the magic wand of natural selection. No need to demonstrate that there is any benefit to the new gene, or that a step-wise path to adaptation exists. Finally, natural selection is especially useful when part of your gene appears unique—since natural selection can change anything, just conclude that natural selection changed your gene so much that it no longer resembles its ancestor.

Gene Evolution Game Rule 3: When a gene seems to be composed of the parts of several genes, just invoke duplications and rearrangements of all the DNA sequences you need, so you can get them all together in the right place. If you need to delete parts of a gene, or invert them, or transpose to a new location, just invoke different types of rearrangements as often and as liberally as you wish, and ba-da-bing, you’ve got your new gene!

And remember, don’t ask those other hard questions. Just use these three rules and you can explain virtually anything. No details required!

References Cited:

[23.] For example, when the ratio of nonsynonymous (i.e. amino acid changing) to synonymous (i.e. non-amino acid changing) differences between Gene B and Gene A is high, we have can say that it must be natural selection at work because only strong selection pressure would preserve so many changes that change amino acid sequence. Incredibly, we can also say that when the same ratio is low (i.e. there are FEW amino acid replacements in a gene), that too shows that natural selection was at work, in this case in the form of stabilizing selection to conserve gene sequence. This approach was taken in Harmit S. Malik and Steven Henikoff, “Adaptive Evolution of Cid, a Centromere-Specific Histone in Drosophila,” Genetics, Vol. 157:1293–1298 (March 2001) and its discussion of the Cid gene in a subsequent post.

[24.] See for example Ulfar Bergthorsson, Keith L. Adams, Brendan Thomason, and Jeffrey D. Palmer, "Widespread horizontal transfer of mitochondrial genes in flowering plants," Nature, Vol. 424:197-201 (July 10, 2003). See also Mark A. Ragan and Robert G. Beiko, "Lateral genetic transfer: open issues," Philosophical Transactions of the Royal Society B, Vol. 364:2241-2251 (2009) (“topological discordance between a gene tree and a trusted reference tree is taken as a prima facie instance of LGT”).

[25.] For example, this explanation was invoked in Matthew E. Johnson, Luigi Viggiano, Jeffrey A. Bailey, Munah Abdul-Rauf, Graham Goodwin, Mariano Rocchi & Evan E. Eichler, “Positive selection of a gene family during the emergence of humans and African apes,” Nature, Vol. 413:514-519 (October 4, 2001).

NOTE: This post is part 5 in a 8-part series responding to the NCSE, Judge Jones, Ken Miller, and the rest of the evolution lobby on the origin of new genetic information. This post, however, is written tongue-in-cheek and should be taken as a parody of the arguments of neo-Darwinists as they attempt to explain the origin of new genetic information. A number of examples showing neo-Darwinists specifically make the mistakes cited in this post will be shown in subsequent posts.

Posted by Casey Luskin at 7:00 AM | Permalink | TrackBacks (1)

Since the close of 2009, Access Research Network (ARN) has released its Top 10 Darwin and Design Science News Stories for 2009 and its Top 10 Media Stories for 2009 (covered recently on the ID the Future podcast – see part 1 and part 2). Now ARN has released its list of the top 10 ID resources for 2009. At the top of the list is Stephen Meyer’s Signature in the Cell: DNA and the Evidence for Intelligent Design. Meyer was not the only Discovery Institute fellow to make ARN’s top 10 resource list. Michael Flannery’s innovative book, Alfred Russel Wallace’s Theory of Intelligent Evolution, and David Berlinski’s long-awaited The Deniable Darwin also made the list.

But there were also a number of excellent resources from authors and groups not affiliated with Discovery Institute. Coming in at second place is Illustra Media’s new documentary, Darwin’s Dilemma: The Mystery of the Cambrian Fossil Record. Another good resource that makes it very high on ARN’s list (#3) is Bradley Monton’s book, Seeking God in Science: An Atheist Defends Intelligent Design. You read that right—Monton is an atheist who finds many ID arguments highly persuasive. Another recommended resource from a new author in the ID-evolution debate is doctor and author James Le Fanu’s book Why Us? How Science Rediscovered the Mystery of Ourselves. We released podcasts with Drs. Monton and Le Fanu last year about their respective books—check out ID the Future to hear the interviews.

Finally, I was quite pleased that two resources I wrote made ARN’s top 10 list. Coming in at number 9 is a law review article published in Hamline University Law Review last year--an attempted exhaustive survey of evolution case law and titled, "Does Challenging Darwin Create Constitutional Jeopardy? A Comprehensive Survey of Case Law Regarding the Teaching of Biological Origins." We've been recounting many of the cases surveyed in that article here on ENV over the past couple months. At number 10 is a lesser-known resource that I’ve nonetheless been getting some positive feedback on -- The College Student’s Back to School Guide to Intelligent Design, a concise FAQ rebutting many common objections that college (or high school) students are likely to hear from their uninformed professors about intelligent design.

Be sure to check out ARN’s Top 10 page to read the lists in full and get links to all of their recommended resources.

Posted by Casey Luskin at 12:00 AM | Permalink | TrackBacks (0)

Despite the fact that proponents of neo-Darwinian evolution claim to understand the origin of new genetic information, they obscure the fact that they lack explanations for such by making vague appeals to mechanisms such as “gene duplication,” “rearrangement,” and “natural selection.” Such mechanisms are generally inferred from circumstantial evidence, i.e. similarities and differences between gene sequences, where a neo-Darwinian evolutionary history is assumed. More importantly, accounts that invoke such mechanisms almost never attempt to assess the likelihood of mutations producing the genetic changes in question. In this regard, important notes of caution must be observed when assessing evolutionary accounts of the origin of a gene.

A 2007 article by evolutionary biologist Michael Lynch in Proceedings of the National Academy of Sciences USA goes to the heart of some of the assumptions inherent in many claims of neo-Darwinian evolution. Lynch provides a list of myths promoted by biologists, and he calls it a “myth” to believe that “Characterization of interspecific differences at the molecular and/or cellular levels is tantamount to identifying the mechanisms of evolution.”¹⁸

Of course, one of the typical “mechanisms of evolution” cited is natural selection, commonly invoked to account for how a gene duplicate acquires a new function. But what kind of evidence is sufficient to demonstrate that positive selection, or natural selection acting to preserve adaptive mutations, has occurred? Biologist Austin Hughes warns that most inferences of positive selection are based upon questionable statistical analyses of genes:

A major hindrance to progress has been confusion regarding the role of positive (Darwinian) selection, i.e., natural selection favoring adaptive mutations. In particular, problems have arisen from the widespread use of certain poorly conceived statistical methods to test for positive selection. Thousands of papers are published every year claiming evidence of adaptive evolution on the basis of computational analyses alone, with no evidence whatsoever regarding the phenotypic effects of allegedly adaptive mutations. … Contrary to a widespread impression, natural selection does not leave any unambiguous ‘‘signature’’ on the genome, certainly not one that is still detectable after tens or hundreds of millions of years. To biologists schooled in Neo-Darwinian thought processes, it is virtually axiomatic that any adaptive change must have been fixed as a result of natural selection. But it is important to remember that reality can be more complicated than simplistic textbook scenarios. … In recent years the literature of evolutionary biology has been glutted with extravagant claims of positive selection on the basis of computational analyses alone ... This vast outpouring of pseudo-Darwinian hype has been genuinely harmful to the credibility of evolutionary biology as a science.¹⁹

In short, evolutionary biologists commonly assume that mutations that change protein sequence were fixed by natural selection, but this assumption may not hold true since many such mutations are neutral and confer no selective advantage.

Biochemist Michael Behe offers another reason not to infer neo-Darwinian mechanisms of change based upon mere evidence of sequence similarity:

Although useful for determining lines of descent ... comparing sequences cannot show how a complex biochemical system achieved its function—the question that most concerns us in this book. By way of analogy, the instruction manuals for two different models of computer put out by the same company might have many identical words, sentences, and even paragraphs, suggesting a common ancestry (perhaps the same author wrote both manuals), but comparing the sequences of letters in the instruction manuals will never tell us if a computer can be produced step-by-step starting from a typewriter. ... Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form? ²⁰

[M]odern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation. ²¹

Many scientific papers purporting to show the evolution of “new genetic information” do little more than identify molecular similarities and differences between existing genes and then tell evolutionary just-so stories of duplication, rearrangement, and subsequent divergence based upon vague appeals to “positive selection” that purport to explain how the gene arose. But exactly how the gene arose is never explained. In particular, whether chance mutations and unguided natural selection are sufficient to produce the relevant genetic changes is almost never assessed. ²² These scientific papers--especially the citation bluffs offered by the NCSE / Judge Jones / Ken Miller--play the Gene Evolution Game, an easy game to play which ultimately tells us little about the origin of new functional genetic information, as we’ll see the next installment of this series.

References Cited:

[18.] Michael Lynch, “The frailty of adaptive hypotheses for the origins of organismal complexity,” Proceedings of the National Academy of Sciences, Vol. 104:8597–8604 (May 15, 2007).

[19.] Austin L. Hughes, "The origin of adaptive phenotypes," Proceedings of the National Academy of Sciences USA, Vol. 105(36):13193–13194 (Sept. 9, 2008) (internal citations removed).

[20.] Michael J. Behe, Darwin's Black Box: The Biochemical Challenge to Evolution, pgs. 175-176 (Free Press, 1996).

[21.] Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism, pg. 95 (Free Press, 2007).

[22.] See for example, “Limits on Evolution” at http://ncseweb.org/creationism/analysis/extrapolations

Posted by Casey Luskin at 9:05 AM | Permalink | TrackBacks (0)

When Judge Jones claimed that Ken Miller showed “the origin of new genetic information by evolutionary processes,” Ken Miller and his friends at the NCSE didn’t just equivocate on the definition of “information,” they also misused the term “new.” In fact, they would likely accept something as “new” if it were merely a copy or a duplicate some pre-existing stretch of DNA, even if the new copy doesn’t actually do anything new, or perhaps even when the new DNA doesn’t do anything at all. In contrast, proponents of intelligent design would define “new” genetic information as a new stretch of DNA which actually performs some different, useful, and new function. For example, consider the following string:

DUPLICATINGTHISSTRINGDOESNOTGENERATENEWCSI

This 42-character string has ~197 bits of Shannon information. Now consider the following string longer:

DUPLICATINGTHISSTRINGDOESNOTGENERATENEWCSIDUPLICATINGTHISSTRINGDOESNOTGENERATENEWCSI

This procedure just added 42 “new” characters, but no new function has been produced. Assuming there was no way to predict beforehand that the first string would be duplicated just as it was, the amount of Shannon information has doubled, but the amount of CSI has not increased one bit (literally).

The above example is of course analogous to the commonly cited evolutionary mechanism of gene duplication, which evolutionists commonly cite as a mechanism by which Darwinian processes can produce new information. But new functional information is not generated by a process of duplication until mutations change the gene enough to generate a new function—which may or may not be possible. As Professor of Neurosurgery Michael Egnor insightfully said in response to one evolutionary biologist:

[G]ene duplication is, presumably, not to be taken too seriously. If you count copies as new information, you must have a hard time with plagiarism in your classes. All that the miscreant students would have to say is 'It's just like gene duplication. Plagiarism is new information- you said so on your blog!'¹⁶

Indeed, evolutionary explanations cannot simply rely upon duplication, for there must be duplication followed by recruitment to a new function. However one defines “information,” merely duplicating a string does not produce new functional information.¹⁷

References Cited:

[16.] Comment by Michael Egnor at http://scienceblogs.com/pharyngula/2007/02/dr_michael_egnor_challenges_ev.php#comment-349555 (February 20, 2007)

[17.] Again, as implied in the body, if one could predict the string would be duplicated, then the Shannon Information would also not increase after duplicating the string, in which case there is no increase in CSI nor Shannon Information.

Posted by Casey Luskin at 10:00 AM | Permalink | TrackBacks (1)

For the NCSE/Ken Miller/Judge Jones to claim that there is an explanation or “the origin of new genetic information by evolutionary processes,” they must equivocate on the definitions of both the words “information” and “new.” Following the NCSE, Judge Jones probably would define information as “Shannon information,” which means mere complexity. Under this definition, a functionless stretch of randomly garbled junk DNA might have the same amount of “information” as a fully functional gene of the same sequence-length. For example, under Shannon information, which the NCSE would claim is “the sense used by information theorists,” the following two strings contain identical amounts of information:

String A:

SHANNONINFORMATIONISAPOORMEASUREOFBIOLOGICALCOMPLEXITY

String B:

JLNUKFPDARKSWUVEYTYKARRBVCLTLODOUUMUEVCRLQTSFFWKJDXSOB

Some leading theorists recognize this point. In 2003, Nobel Prize winning origin of life researcher Jack Szostak wrote in a review article in Nature lamenting that the problem with “classical information theory” is that it “does not consider the meaning of a message” and instead defines information “as simply that required to specify, store or transmit the string.”¹¹ According to Szostak, “a new measure of information – functional information – is required” in order to take account of the ability of a given protein sequence to perform a given function. Likewise, a paper in the journal Theoretical Biology and Medical Modelling observes:

[N]either RSC [Random Sequence Complexity] nor OSC [Ordered Sequence Complexity], or any combination of the two, is sufficient to describe the functional complexity observed in living organisms, for neither includes the additional dimension of functionality, which is essential for life. FSC [Functional Sequence Complexity] includes the dimension of functionality. Szostak argued that neither Shannon’s original measure of uncertainty nor the measure of algorithmic complexity are sufficient. Shannon's classical information theory does not consider the meaning, or function, of a message. Algorithmic complexity fails to account for the observation that “different molecular structures may be functionally equivalent.” For this reason, Szostak suggested that a new measure of information—functional information—is required.¹²

In 2007 Szostak co-published a paper Proceedings of the National Academy of Sciences with Carnegie Institution origin of life theorist Robert Hazen and other scientists furthering these arguments. Attacking those who insist on measuring biological complexity using the outmoded tools of Shannon information, the authors wrote, “A complexity metric is of little utility unless its conceptual framework and predictive power result in a deeper understanding of the behavior of complex systems.” Thus they “propose to measure the complexity of a system in terms of functional information, the information required to encode a specific function.”¹³

Stephen C. Meyer follows this approach, writing in a peer-reviewed scientific paper that it is useful to adopt “‘complex specified information’ (CSI) as a synonym for ‘specified complexity’ to help distinguish functional biological information from mere Shannon information—that is, specified complexity from mere complexity.”¹⁴ Meyer’s suggested definition of “specified complexity” is useful in describing functional biological information. Specified complexity is a concept derived from the mainstream scientific literature and is not an invention of critics of neo-Darwinism. In 1973, origin of life theorist Leslie Orgel distinguished specified complexity as the hallmark of biological complexity:

[L]iving organisms are distinguished by their specified complexity. Crystals are usually taken as the prototypes of simple, well-specified structures, because they consist of a very large number of identical molecules packed together in a uniform way. Lumps of granite or random mixtures of polymers are examples of structures which are complex but not specified. The crystals fail to qualify as living because they lack complexity; the mixtures of polymers fail to qualify because they lack specificity. ¹⁵

Orgel thus captures the fact that specified complexity, or CSI, requires both an unlikely sequence and a specific functional arrangement. Specified complexity is a much better measure of biological complexity than Shannon information, a point which the NCSE must resist because it’s much harder to generate specified complexity via Darwinian processes than mere Shannon complexity.

By wrongly implying that Shannon information is the only “sense used by information theorists,” the NCSE avoids answering more difficult questions like how the information in biological systems becomes functional, or in its own words, “useful.” Rather, the NCSE seems more interested in addressing simplistic, trivial questions like how one might add additional characters to a string, or duplicate a string, without regard for the all important question of whether those additional characters convey some new functional message. Since biology is based upon functional information, Darwin-skeptics are interested the far more important question of, Does neo-Darwinism explain how new functional biological information arises?

References Cited:
[9.] This calculation uses a 26 letter English alphabet that is not case-sensitive and, as seen in the strings, does not use spaces.

[10.] String B was generated using a random character generator from the website Random.org.

[11.] Jack W. Szostak, “Molecular messages,” Nature, Vol. 423:689 (June 12, 2003).

[12.] Kirk K. Durston, David K. Y. Chiu, David L. Abel, Jack T. Trevors, “Measuring the functional sequence complexity of proteins,” Theoretical Biology and Medical Modelling, Vol. 4:47 (2007) (internal citations removed).

[13.] Robert M. Hazen, Patrick L. Griffin, James M. Carothers, and Jack W. Szostak, "Functional information and the emergence of biocomplexity," Proceedings of the National Academy of Sciences, USA, Vol. 104:8574–8581 (May 15, 2007).

[14.] Stephen C. Meyer, “The origin of biological information and the higher taxonomic categories,” Proceedings of the Biological Society of Washington, Vol. 117(2):213-239 (2004).

[15.] Leslie E. Orgel, The Origins of Life: Molecules and Natural Selection, pg. 189 (Chapman & Hall: London, 1973).

Posted by Casey Luskin at 9:07 AM | Permalink | TrackBacks (1)

Last Thursday night I spoke at the University of Arkansas for an Academic Freedom Day Event. The crowd was civil with a good mix of both ID-friendly folks and ID-skeptics. The Q & A was generally harmless but the most amusing question of all came from a very nice gentleman with a local "Free Thinkers" group who asked me a 'how dare you' type question, arguing that because the “consensus” or "thousands" of scientists oppose ID, so should I.

Here’s a little snippet of what I said in reply: “ID is a minority scientific view. But you owe it to yourself to examine the issue for yourself and come up with your own viewpoint. And if the consensus is right, fine. If it’s wrong, fine. But if you are just going to dismiss ID because somebody else tells you to then you have fallen into an anti-intellectual position.”

So it turns out that the "Free thinkers" don't really think you should be free to think for yourself when it comes to evolution. In their view, you should just think what certain scientists tell you to think. Who would have thought?

Posted by Casey Luskin at 9:30 AM | Permalink | TrackBacks (0)

The Journal of Eukaryotic Microbiology recently published several papers from a workshop sponsored by the International Society of Protistologists titled “Horizontal Gene Transfer and Phylogenetic Evolution Debunk Intelligent Design.” So here we have a respected scientific society, presumably planning a workshop months in advance, and finally laying out their considered case for why intelligent design fails. As you might imagine, I was most anxious to read about it. Unfortunately, rather than scholarly papers, the manuscripts read like press releases from the National Center for (Darwinian) Science Education. So the introductory essay¹ by Avelina Espinosa tells us that ID has “creationist beginnings,” claims that I say “evolution” is “impossible,” and places in my mouth the phrase “design creationism” (I have never uttered that phrase except to disparage it). Blah, blah, blah. About as much scholarship as you’d get from a typical politician.

The first of the full articles² concerned itself mostly with common descent, which I have always said I think is correct, and which in any case is not an issue of intelligent design. Another article, however, briefly dealt with my case from The Edge of Evolution, that some adaptations are likely to require multiple mutations, and thus be very improbable.* In “Using Protistan Examples to Dispel the Myths of Intelligent Design”³ University of Georgia Professor Mark Farmer and Wadsworth Center Dr. Andrea Habura start off sloppily: “According to Behe (2007), the odds that mutations required to impart chloroquine resistance in Plasmodium could arise naturally are so impossibly long that they lie beyond what he considers ‘’The Edge of Evolution.’” But the book clearly states that chloroquine resistance in Plasmodium did arise naturally, by Darwinian processes. I go on to argue it took very many malarial parasites to chance upon resistance, and that pointed to a limit for Darwinian evolution for more complex mutations, or for populations with smaller numbers than Plasmodium, but I clearly said the opposite of what Farmer and Habura³ ascribe to me, that chloroquine resistance arose naturally. That doesn’t give a reader confidence that the authors concern themselves much with the details of an argument.

Farmer and Habura think I am wrong that multiple mutations were necessary in the protein PfCRT to confer chloroquine resistance on malaria. They think only one will suffice. What’s more, they claim there are experiments to show that. They cite two papers.³⁴ But neither paper even tries to test whether a single mutation in PfCRT confers chloroquine resistance. Lakshamana et al. (2005) show that if they remove one particular mutation (K76T) from a mutant protein that carried a half dozen or so other mutations (compared to the wild-type protein), the protein no longer confers chloroquine resistance. That experiment shows the K76T is necessary; however, it does not show it is sufficient by itself, as Farmer and Habura thought. The same goes for the second paper. In their methods section Jiang et al (2008) write that “Parasite 106/1^K76 [a chloroquine-sensitive strain that does not have the K76T mutation] has six mutations found typically in Southeast Asian CQR parasite ... except a key mutation at PfCRT 76 position.”) Thus both these papers show that K76T is necessary, but neither shows it to be sufficient. To do so one would have to test the K76T in the wild-type, unmutated background.

To recap, several years after The Edge of Evolution was published a scientific society held a workshop to demonstrate the book’s errors. Yet they couldn’t even get the book’s argument straight, and the experimental work they cited against my argument is not even pertinent to it. Apparently the design argument drives some scientists so much to distraction that they lose their normally robust powers of reasoning.

Footnote
*Most of the second paper actually dealt with making a case for macroevolution based on a series of fossil foraminifera. Whether or not one wishes to classify the series as an example of “macroevolution,” the accompanying drawings are not likely to persuade skeptics, and in any event are at the anatomical level rather than the molecular level, where, I have always argued, one must look to determine whether an evolutionary event is feasible by Darwinian processes.

References
¹ Espinosa, A. 2010. Introduction: protistan biology, horizontal gene transfer, and common descent uncover faulty logic in intelligent design. J. Eukaryot. Microbiol. 57:1-2.
² Paz, Y. M. and Espinosa, A. 2010. Integrating horizontal gene transfer and common descent to depict evolution and contrast it with "common design". J. Eukaryot. Microbiol. 57:11-18.
³ Farmer, M. A. and Habura, A. 2010. Using protistan examples to dispel the myths of intelligent design. J. Eukaryot. Microbiol. 57:3-10.
⁴ Lakshmanan, V., Bray, P. G., Verdier-Pinard, D., Johnson, D. J., Horrocks, P., Muhle, R. A., Alakpa, G. E., Hughes, R. H., Ward, S. A., Krogstad, D. J., Sidhu, A. B., and Fidock, D. A. 2005. A critical role for PfCRT K76T in Plasmodium falciparum verapamil-reversible chloroquine resistance. EMBO J. 24:2294-2305.
⁵ Jiang, H., Patel, J. J., Yi, M., Mu, J., Ding, J., Stephens, R., Cooper, R. A., Ferdig, M. T., and Su, X. Z. 2008. Genome-wide compensatory changes accompany drug- selected mutations in the Plasmodium falciparum crt gene. PLoS. One. 3:e2484.

Posted by Michael Behe at 12:32 PM | Permalink | TrackBacks (0)

Intelligent design (ID) has attracted its fair share of critics. If it’s not the fulminations of New Atheists, it’s extremely uncharitable readings from some Catholic intellectuals who think they smell mechanism or interventionism. While the criticisms vary, they tend to have one thing in common: they’re based, not on actual ID arguments, but on stereotypes and misunderstandings of those arguments. It’s hard to find ID critics who actually describe an ID argument correctly before proceeding to refute it.

Catholic physicist Stephen Barr is a constitutionally uncharitable critic of ID. It’s not clear that he has even read the books that he criticizes. But he criticizes them nonetheless.

In a February 9 diatribe in First Things, he makes several complaints. For instance, he asserts, bizarrely, that ID claims that science is incompetent. He faults ID for effectively disagreeing with Bacon on the arbitrary rule that “science” can’t consider intelligence or purpose, implying that this somehow puts ID at odds with the Catholic tradition, even though science for St. Thomas and the Catholic tradition generally was never limited to a positivistic rendering of natural science. He faults ID for not using the same examples of design used by the author of the Book of Wisdom around 100 B.C. He claims, without evidence, that “very few religious skeptics have been made more open to religious belief because of ID arguments.” (How could he possibly know that?)

And he offers this stereotypical complaint, to which ID proponents have responded ad nauseam:

The ID movement’s version (of the design argument) is hostage to every advance in biological science. Science must fail for ID to succeed. In the famous “explanatory filter” of William A. Dembski, one finds “design” by eliminating “law” and “chance” as explanations. This, in effect, makes it a zero-sum game between God and nature. What nature does and science can explain is crossed off the list, and what remains is the evidence for God. This conception of design plays right into the hands of atheists, whose caricature of religion has always been that it is a substitute for the scientific understanding of nature. The ID movement’s version (of the design argument) is hostage to every advance in biological science. Science must fail for ID to succeed. In the famous “explanatory filter” of William A. Dembski, one finds “design” by eliminating “law” and “chance” as explanations. This, in effect, makes it a zero-sum game between God and nature. What nature does and science can explain is crossed off the list, and what remains is the evidence for God. This conception of design plays right into the hands of atheists, whose caricature of religion has always been that it is a substitute for the scientific understanding of nature. ¹

Anyone familiar with ID will know that Barr is simply defining science to exclude consideration of intelligence, whereas the burden of ID is arguments is to show that intelligence is within the purview of science properly construed. But rather than going into all that, let’s just focus on Barr’s theological complaint against ID, since it’s quite common.

Admittedly, the way some ID proponents speak can lead to misunderstandings, if read uncharitably. When discussing biology, for example, ID theorists frequently contrast the role of natural laws like gravity with the role of intelligent design. They may speak of natural selection as a “mindless” or “brute” or even “purposeless” process. To the grumpy reader interpreting this language theologically, this can sound like ID implies that God only acts apart from these natural forces, that he is merely an artificer who rearranges pre-existing material, that there are forces in the world that seem to exist apart from God’s activity, or that God only acts where nature leaves off. God’s action, then, would be set up against nature, and left to fill the “gaps” that nature leaves empty.

These ideas would certainly be problematic, as Barr charges, if anyone actually advanced them; but no theistic ID proponent ever has. No theist worth his salt believes that God is aloof from the world except when he acts directly in nature. That would be a sort of modified deism—though, strictly speaking, deists don’t think God acts within the world at all. For theists, in any case, God transcends the world, is free to act directly in it—however unfashionable that might be—and always remains intimately involved with it.

At the same time, the theist need not believe that God always acts directly in the world. He can act directly or “primarily,” such as when he creates the whole universe or raises Jesus from the dead. It’s God’s world, so that’s his prerogative. He’s not violating the universe or its laws, or invading alien territory when he does this, since he’s the source of both the universe and whatever “laws” it might have.

He also can act through so-called “secondary causes.” These include natural processes and laws that he has established, such as the electromagnetic force. (I think it’s problematic to speak of physical constants as “causes,” but let that pass for now). An event might be both an expression of a physical law and the purposes of God. It’s not as if atheists appeal to gravity while theists appeal to miracles. Gravity is as consistent with theism as are miracles. It’s just that most theists and atheists agree on gravity but not on miracles.

When an ID theorist in question is also a theist, then these distinctions are always in the background, even if they don’t show up in every argument. That’s because ID arguments often focus on discrete, empirical evidence of design in nature—that is, with “design” insofar as it is detectible and tractable in an open-minded scientific framework. This is nothing new. While St. Thomas made broad design arguments, he also pointed to specific examples of design within nature. ID theorists simply point to evidence that Thomas knew nothing about.

Consider Mike Behe. When he is discussing the bacterial flagellum, he is evaluating the powers and limits of regular, repetitive physical laws (or, as I would say, of matter insofar as it acts according to these laws), and of the Darwinian “mechanism”—natural selection and random genetic mutation. He concludes that these processes, which are not intelligent agents per se, probably don’t have the power, by themselves, to produce the bacterial flagellum. That’s because the locomotive function of the flagellum is inaccessible to the cumulative power of natural selection. It is, as Behe says, “irreducibly complex.” It needs many separate parts working together before it gets the survival-benefitting function. That’s the negative part of his argument.

To get a working flagellum, according to Behe, you need foresight—the exclusive jurisdiction of intelligent agents. That’s the positive part of his argument—not just against the adequacy of selection and mutation, but for intelligent design. An agent can produce a system for a future purpose, for an end. Now it’s the obvious purpose of the flagellum, along with the fact that it is almost surely inaccessible to Darwinian selection—not merely the fact that it’s really complicated—that justifies his conclusion that the bacterial flagellum is better explained by intelligent design than by repetitive natural laws or the Darwinian mechanism.

Behe makes a similar argument with respect to the biochemical cascade in a light-sensitive spot, from which, say, the mammalian eye putatively evolved by Darwinian means. Behe focuses on the light sensitive spot, not because he thinks the entire eye is easily accessible to Darwinian mechanism, but because the eye depends for its function on the simpler light sensitive spot, which is well-understood and tractable.

But it’s a misunderstanding to construe Behe’s arguments as complete descriptions of what God is doing. He is talking about detectible design in a subfield of biology, in which physical constants are treated as given, and the limits of mutation and natural selection can be discerned. In the case of the bacterial flagellum, intelligent design goes beyond what known, repetitive, natural processes, as well as selection and mutation would do if left to their ordinary capacities. So we invoke intelligent design rather than impersonal processes alone here. Contrary to Barr’s argument-free assertions, this is not an appeal to go “beyond science” or a claim that science is incompetent. It’s an argument for why science ought to include teleology within its explanatory toolbox if it wants to adequately account for major aspects of nature.

That’s how the design argument works here; but it’s not how every design argument, focusing on every feature of nature, works.

Ordinarily, when a scientist invokes a physical law, he intends to appeal to some fixed feature of the physical world. A ball falls to the ground when dropped from the Leaning Tower of Pisa “because” of gravity. So a scientist can say that gravity “causes” the ball to fall (once dropped). (Again, I think this way of speaking is misleading, but it’s conventional so I won’t challenge it.) Since it’s constant—it always does the same, mathematically describable thing—and isn’t an intelligent agent, gravity is seen as an impersonal property of matter. But that doesn’t mean the scientist intends to exclude God’s role in some broader sense, or that God is so excluded whatever the scientist intends. The scientist has simply taken gravity as a given fact about the natural world.

Similarly, Behe’s argument does not imply that nature is a self-contained entity going on its merry way except when God decides to jump in to build a bacterial flagellum. Nor is Behe implying that natural laws or so-called impersonal processes are outside God’s purposes or control. Nor is he saying anything about the value of other teleological arguments—such as Thomas’s Fifth Way. He’s simply talking about detecting design in tiny domains of biology that we understand well, and treating impersonal constants and mechanisms, such as gravity and the Darwinian mechanism, as givens. ²

The Wrong Kind of Design Argument?

Stephen Barr offers another common complaint, which is that ID is quite different from the design argument made by the Church Fathers and scholastics:

The emphasis in early Christian writings was not on complexity, irreducible or otherwise, but on the beauty, order, lawfulness, and harmony found in the world that God had made. ³

Barr seems to imply that there’s some theological problem with appealing to certain kinds of complexity; but obviously there is not. The Church Fathers didn’t talk about bacterial flagella or DNA because they didn’t know anything about them.

In any case, this complaint is also based on a misunderstanding. Neither Behe’s nor any other ID argument implies that other design arguments are illicit. From a different vantage point, the “fine tuning” of physical constants may itself be evidence for intelligent design. There’s no zero-sum game here. It’s not as if gravity and electromagnetism are points for the materialist, whereas the bacterial flagellum is a point for the theists. It’s just that we might only notice the “designedness” of physical constants when we attend to them directly. In biology, physical constants are often part of the background. That’s true of Behe’s argument, as well as of Steve Meyer’s argument concerning biological information. But the background is interesting too.

Think of it this way. Imagine an expedition of future astronauts is exploring a distant planet. They find something that looks like a book with pages, which look like they contain written text. The language is unique; no one has ever seen it before; and the “book” is quite exotic. So it’s given to a crack team of exoplanet cryptographers, who eventually determine that it is in a fact a book—a cookbook. Now they know that the text was written by intelligent beings. They would not have been able to determine that without focusing on the text, and treating the pages, binding, and cover as background contrasts to the text. But once they decrypt the text, they could then turn their attention to the book itself. Noting its chemical composition, artful design, and user-friendly layout, they would then realize that the book itself, and not just the text, is the product of intelligence.

In the same way, one can make a design argument based on some narrow feature in the biological world without denying that the background media, considered on their own, are also evidence of design. ID theorists do that all the time. They point to evidence for design from physics and cosmology. And they appeal to beauty and rationality in nature as evidence for design. ID is not an either-or approach, but rather a both-and.⁴

In fact, some recent design arguments go well beyond biological function and its constraints. Guillermo Gonzalez and I, for instance, developed a design argument based on evidence ranging from geology to astronomy and cosmology suggesting that the universe appears to be designed not just for intelligent life but also for scientific discovery.⁵ It’s very hard to see how such an argument is anti-science, as Barr suggests.

Of course, as with the case of the book and text, even if, say, fine tuning in physics is evidence of design, it doesn’t follow that the fine-tuning of, say, gravity and electromagnetism are adequate to give rise to reproducing cells or other things we discover in nature. There’s no theological principle that requires otherwise. In fact, we may still detect design at the cellular level in part by contrasting it with the background regularities of physics. It would then be an example of what philosopher Del Ratzsch calls “counterflow”⁶ : it exhibits features we have good reason to doubt can be produced by ordinary, repetitive physical processes, but that could be produced by an intelligent agent. Pointing to evidence of counterflow is no insult to physics or to God, anymore than saying that gravity alone couldn’t produce Shakespeare’s sonnets is no insult to gravity—though it might be an insult to Shakespeare.

I should add that even if we can’t render a stand-alone design argument from some narrow aspect of nature, it doesn’t follow that God is not still in charge of that part of nature, or that it might not still be the occasion for someone to see or experience God. Scientific study is not the only way to experience or gain knowledge of nature. But it is one way. And if there is evidence of design in that realm that natural scientists study, then there’s no good reason, either philosophical or theological, why they shouldn’t be free to consider it.

Again, Barr’s complaints are so varied and scattered that it’s cumbersome to respond to them all in one place. But if he’s going to be a career critic of ID, perhaps he might actually read the books by ID proponents, and critique those, rather than continue to offer these angry drive-by shots based on his misinterpretations.

Notes
¹ Stephen Barr, “The End of Intelligent Design?” First Things (February 9, 2010), at: http://www.firstthings.com/onthesquare/2010/02/the-end-of-intelligent-design. Obscurely, after his diatribe, Barr admits: “None of this is to say that the conclusions the ID movement draws about how life came to be and how it evolves are intrinsically unreasonable or necessarily wrong.”
² Behe discusses this issue in “God, Design, and Contingency in Nature” (Nov. 12, 2009), at: http://www.evolutionnews.org/2009/11/god_design_and_contingency_in.html.
³ Barr, “The End of Intelligent Design?”
⁴ For discussion of beauty as evidence of design, see Benjamin Wiker and Jonathan Witt, A Meaningful World: How the Arts and Sciences Reveal the Genius of Nature (Downers Grove: InterVarsity Press, 2006).
⁵ See, for instance, Guillermo Gonzalez and Jay W. Richards, The Privileged Planet: How Our Cosmos is Designed for Discovery (Washington DC: Regnery, 2004), and Stephen C. Meyer, “The Return of the God Hypothesis,” available online at: http://www.discovery.org/articleFiles/PDFs/ReturnofGdHypth.pdf.
⁶ Del Ratzsch, Nature, Design, and Science (Albany: State University of New York Press, 2001).

Posted by Jay Richards at 8:59 AM | Permalink | TrackBacks (0)

Darwin was wrong.
Missing links still missing.
There is no such thing as junk DNA.
Birds did not descend from Dinosaurs.
Irreducible complexity is still irreducibly complex.
Tiktaalik has been invalidated by an earlier ancestor.
Haeckel’s embryo drawings are still fake (and still in textbooks).

Yet, evolution is a fact?

Posted by Robert Crowther at 1:18 PM | Permalink | TrackBacks (1)

There’s a disturbing trend for the role of media in a democracy: journalists who don’t trust their profession, the public, or themselves. These days more reporters, editors, and journalism advocates are urging their colleagues to jettison objectivity in reporting and replace it with something they can trust: their blind allegiance to authority.

Perhaps no one serves as a better example of this than New York Times science writer Cornelia Dean. Her new book, Am I Making Myself Clear?: A Scientist's Guide to Talking to the Public, has a gem of a chapter titled “The Problem of Objectivity.”

You read that correctly. Here’s a journalist who sees objectivity as a problem. To wit:

In striving to be “objective” journalists try to tell all sides of the story. But it is not always easy for us to tell when a science story really has more than one side — or to know who must be heeded and who can safely be ignored. When we cast too wide a net in search of balance, we can end up painting situations as more complicated or confusing than they really are. (pp. 47-48, emphasis added)

You can think of plenty of examples of such stories: climate change (it’s real, and people are contributing to it); HIV and AIDS virus (the virus does cause the disease); vaccine preservatives as a cause of autism (not). In each case, though, there are prominent people, some with respectable technical credentials, supporting the so-called dissident view. President Bush was a prominent climate-change denier, and it is difficult for a conventional American journalist to say any president is flat-out wrong. (p. 48, emphasis added)

Of course, if that’s the case, the rest of this chapter becomes utter nonsense. Dean’s point is that journalists can’t get science, so they have to be careful and trust only the scientists whom scientists respect (and yes, that is some pretty swell circular logic she’s got going for her). Just know that, if you’re a journalist, you’re not going to be able to judge for yourself. Don’t worry about it and remember that at least you’re a journalist and not a plebian member of the American public:

The point is, debate and disagreements are hallmarks of science, especially in arenas where science and policy intersect. Journalists will be hard-pressed to tell the good idea from the specious. And when we journalists are unable (or unwilling) to judge for ourselves, we often fall back on he-said-she-said reporting. In effect, we turn the whole question over to our readers (or listeners or viewers), who probably have even less basis for judgment than we do. (p. 52)

Not Dean. If she doesn’t think the public can grasp the science at hand, she also doesn’t trust the journalist either. It’s a false humility, one designed to tell her colleagues where they should turn when they can’t make the judgment calls themselves (judgment they only have to make because they don’t trust the people they report to, remember): throw up your hands and appeal to a higher power, namely the authority of the Establishment.

This problem of objectivity has no ready solution. For me it is by far the most intractable problem in coverage of science and engineering. In my opinion, scientists and engineers are the only ones who can help solve it. (p.55)

Posted by Anika Smith at 8:30 AM | Permalink | TrackBacks (0)

Not long before the beginning of the 2005 Kitzmiller v. Dover trial, then-National Center for Science Education staff member Nicholas Matzke told a reporter, “The origin of genetic information is thoroughly understood.” ¹ During the Dover trial, plaintiffs’ expert witness, biologist Kenneth Miller, testified that he presented Judge John E. Jones with “more than three dozen scientific studies showing the origin of new genetic information by these evolutionary processes.” ² The plaintiffs’ attorneys, working with the NCSE, successfully convinced Judge Jones to parrot Miller by stating in the Kitzmiller v. Dover ruling that Miller had “pointed to more than three dozen peer-reviewed scientific publications showing the origin of new genetic information by evolutionary processes.” ³

Virtually all of those “publications” mentioned by Judge Jones came from one single paper Miller discussed at trial, a review article, co-authored by Manyuan Long of the University of Chicago.⁴ The article does not even contain the word “information,” much less the phrase “new genetic information.” ⁵

The NCSE continues to cite Long et al. claiming that the origin of new functional biological information is nothing to be troubled about. Last year NCSE posted an online response to parts of Explore Evolution: The Arguments For and Against Neo-Darwinism (“EE”), stating that “Biologists have no trouble showing how new information (in the sense used by information theorists) originates, nor how new genes, kinds of cells or tissues evolve.” Similar arguments appear in an article co-authored by former NCSE staff member Matzke critiquing critical analysis of evolution. Matzke writes with Paul Gross that it is “scandalously wrong” to argue that modern evolutionary biology has had difficulty accounting for the origin of new biological information because “[c]ompetent scientists know how new genetic information arises.”⁶ He too relies upon the paper by Long et al. asserting that “it reviews all the mutational processes involved in the origin of new genes and then lists dozens of examples in which research groups have reconstructed the genes’ origins.”⁷

But are Judge Jones’s, Ken Miller’s, and the NCSE’s bold proclamations supported? Does Long et al. actually reveal the origin of new biological information? Is Explore Evolution wrong? A closer look shows that the NCSE is equivocating over the meanings of the words “information” and “new,” and that the NCSE’s citations are largely bluffs, revealing little about how new genetic functional information could originate via unguided evolutionary mechanisms. This bluff was accepted at face value by Judge Jones, who incorporated it in his highly misguided legal ruling.

In fact the origin of new functional biological information is perhaps the most important question in biology. As origin of life theorist Bernd-Olaf Kuppers stated in his book Information and the Origin of Life, “The problem of the origin of life is clearly basically equivalent to the problem of the origin of biological information.”⁸

Judge Jones was not merely in error. Worse than any simple mistake, the misinformation he propounded in his ruling entered media and academic culture, becoming enshrined as a Darwinian myth, alongside many others. This myth holds that perhaps the most important question in biology has been solved, when really (as this series of 8 total posts will show), that is far from being the case.

References Cited:

[1.] Nicholas Matzke quoted in Michael Powell, “Controversial Editor Backed,” Washington Post (August 19, 2005).

[2.] Kenneth R. Miller, Kitzmiller v. Dover Day 1 AM testimony, pg. 135 (September 26, 2005).

[3.] Kitzmiller v. Dover, 400 F.Supp.2d 707, 744 (M.D.Pa. 2005).

[4.] Manyuan Long, Esther Betrán, Kevin Thornton, and Wen Wang, “The Origin of New Genes: Glimpses from the Young and Old,” Nature Reviews Genetics, Vol. 4:865-875 (November, 2003).

[5.] The word “information” appears once in the entire article—in the title of note 103. Id. at 875 n. 103. See Manyuan Long, Esther Betrán, Kevin Thornton, and Wen Wang, “The Origin of New Genes: Glimpses from the Young and Old,” Nature Reviews Genetics, Vol. 4:865-875 (November, 2003).

[6.] Nicholas J. Matzke and Paul R. Gross, “Analyzing Critical Analysis: The Fallback Antievolutionist Strategy,” pg. 42 in Not in Our Classrooms: Why Intelligent Design is Wrong for Our Schools (edited by Eugenie C. Scott and Glenn Branch, Beacon Press, 2006).

[7.] Id.

[8.] Bernd-Olaf Kuppers, Information and the Origin of Life (Cambridge: MIT Press, 1990), pp. 170–172.

Posted by Casey Luskin at 8:14 AM | Permalink | TrackBacks (2)

Academic freedom week is about more than quoting Darwin and maybe watching an appropriate film for the occasion. (No, not that one. That one’s boring. This one.) It’s about the scientists, scholars, journalists, teachers and students who are affected when fear of inquiry rears its ugly head in the debate over evolution. When you hear the stories of ordinary men and women who have been targeted in this battle over an idea, the importance and impact of the debate becomes clear.

So you’re informed about the issues — you read the blog, listen to the podcast, get the newsletter, and stay involved in the debate as it continues. What else can you do?

If you’re a college or graduate student, you can learn even more about intelligent design. In fact, you can get equipped and be inspired to join the movement.

Discovery Institute has two intensive summer seminars on intelligent design, science, and culture from July 9-17, 2010 in Seattle. The first seminar is for students in the natural sciences and philosophy of science; the second seminar is for students in the social sciences and humanities (including politics, law, journalism, and theology).

These seminars are designed for highly-motivated college students who seek a deeper understanding of science and its implications for society. The seminar focusing on ID in the natural sciences will explore the scientific issues in greater technical detail and the seminar on ID in the social sciences and humanities will give more in-depth attention to the social impact of science. This year’s seminar will feature Michael Behe, Douglas Axe, Stephen Meyer, Jay Richards, and many other leading lights in the intelligent design community.

Discovery Institute will pay expenses for students who are accepted into this special program (travel, lodging, meals, books and other course materials). Applications will be accepted until April 16, 2010, but earlier applications may receive priority consideration. Click here for more information.

If you’re not a student, please consider forwarding this information on to the students you know who may be interested. Who knows? They may end up becoming the next Michael Behe or Stephen Meyer.

Posted by Anika Smith at 3:15 PM | Permalink | TrackBacks (0)

Just in time for Academic Freedom Day, Feb. 12 (aka Darwin Day), graduate student Michael Barton at Montana State University boasts of regularly going into his local bookstore and purging books critical of Darwin from the science section of the store and reshelving them in the religion section. This past Sunday Barton posted a report about his most recent act of vandalism:

Today I moved [Michael Behe’s] The Edge of Evolution and [Benjamin Wiker’s] The Darwin Myth away from the shelve directly under where copies of Dawkins’s The Greatest Show on Earth were, and placed them next to--I just had to--the Adventure Bible and the Princess Bible in the religion section.

Whatever Barton claims, his actions constitute censorship, pure and simple. Barton is trying to hide books he doesn’t like in order to prevent others from being exposed to views with which he disagrees. Indeed, he is apparently so insecure about the ability of Darwinists like Dawkins to make their case that he thinks he has the duty to vandalize private bookstores in order to keep the books of Darwin’s critics away from the public. Barton’s activities are not only juvenile, they may well be illegal.

Censors like Barton aren’t doing Darwinian evolution any favors. They merely prove to the public just how bigoted and intolerant the Darwinist establishment has become. Much like certain global warming fanatics, Darwinist ideologues increasingly place themselves above the law and try to exempt themselves of any sort of real accountability.

Ironically, Darwin himself was a lot more fair-minded than his latter-day defenders. Writing at the beginning of On the Origin of Species, Darwin acknowledged that “a fair result can be obtained only by fully stating and balancing the facts and arguments on both sides of each question.”

Posted by John West at 1:43 AM | Permalink | TrackBacks (0)

Over at Biologic Institute, Director Douglas Axe highlights a new paper that brings clarity to the origin of life debate.

The paper’s title is a diplomatic statement of its main conclusion: Lack of evolvability in self-sustaining autocatalytic networks constrains metabolism-first scenarios for the origin of life. It becomes clear on reading the paper that the word constrains is here being used euphemistically

At the time, my work was focusing on the profound differences between the simple catalysis caused by small molecules and the elaborately orchestrated and stunningly efficient catalysis achieved by enzymes—the catalysts of life. Kauffman was equating complexity with the sheer numbers of chemical species and reactions, whereas my concern was with the mode of reaction. Since Kauffman’s model employed reactions that were fundamentally simple, with no discernible prospect of rising above this, I saw no satisfactory connection between his model and life.

But the difficulty of explaining life’s origin makes even hints of progress a big deal, and many saw in Kauffman’s simple model the potential for something bigger. The reason for their optimism, I think, was expressed by Daniel Dennett around the time of Kauffman’s writing: “Evolution will occur whenever and wherever three conditions are met: replication, variation (mutation), and differential fitness (competition).” The hope was that if autocatalytic networks can deliver those three things, then whatever they lack in comparison to modern life they can acquire through progressive evolution.

I think it’s fair to say that the optimism has faded as the years have passed without anything like a convincing demonstration—at least nothing that could be called “autocatalytic metabolism.” Now it seems things may be drawing to a close with a new paper by Vasas, Szathmáry, and Santos. Their work calls this whole notion of life starting with raw metabolism into question by seriously undermining the biological relevance both of Kauffman’s conjecture and of Dennett’s dictum.

Posted by Anika Smith at 2:06 PM | Permalink | TrackBacks (0)

A new website has just launched in support of Dr. Granville Sewell's new book, In The Beginning and Other Essays on Intelligent Design. Along with information about the book, there is a nice brief interview with Sewell that you will want to read.

Q. You express some doubt that even under “the right conditions, the influx of stellar energy into a planet could cause atoms to rearrange themselves into nuclear power plants and spaceships and computers.” This, you say, ought to be “considered an open question” at least by scientists and the public alike. Why isn’t it?

A. A typical college physics text I read contains the statement “One of the most remarkable simplifications in physics is that only four distinct forces account for all known phenomena.” Most people just haven’t ever thought about things in this way, that if you don’t believe in intelligent design, you must believe this claim, that the four unintelligent forces of physics caused atoms on Earth to rearrange themselves into nuclear power plants, spaceships and computers. When they do think about it, they may start to see things a little differently. This is part of the “broader view” that is often missed by biologists, but noticed by mathematicians and physicists.

Also, a heads up for those of you in Seattle. Dr. Sewell will be presenting his book at Discovery Institute on February 23rd. And for everyone else, next week ID The Future will podcast two interviews with Dr. Sewell about his views on intelligent design, origin of life theories, and why he thinks Darwin's theory about the struggle for life "easily the dumbest idea ever taken seriously by science."

Posted by Robert Crowther at 9:00 AM | Permalink | TrackBacks (0)

It's that time of year! ID the Future just kicked off a series of podcasts for Academic Freedom Week, taking a look back over the academic freedom stories in the media last year and a look ahead to the current struggles for academic freedom in the debate over evolution and intelligent design.

Leading off was today's interview of ARN Executive Director Dennis Wagner, who discussed with Casey Luskin the expelling of Ben Stein from the University of Vermont, the censorship of Michael Behe's Bloggingheads.tv interview, and the lawsuit against the California Science Center over their cancellation of the pro-ID film, Darwin’s Dilemma.

Stay tuned to the entire series of podcasts this week at IDtheFuture.com.

Posted by Anika Smith at 4:16 PM | Permalink | TrackBacks (0)

Jerry Fodor and Massimo Piatelli-Palmarini are arrving late to the Darwin doubting party, but are welcome attendees none the less. Below are some welcoming remarks from leading scientific voices in the intelligent design community.

We just received a review copy of "What Darwin Got Wrong", the new book attacking Darwinian evolution by Jerry Fodor and Massimo Piatelli-Palmarini, two thorougly materalistic scientists. Why does that matter? Because typically materialists have been the most ardent defenders of Darwin's theory of natural selection. With the publication of this book, that is likely to change.

For those of you wondering what this is all about let me back up to 2007 when Fodor published his first piece of heresy in the London Review of Books, "Why Pigs Don't Have Wings". That article led to Stanley Salthe, another materialist scientist who doubts Darwrinian evolution (and has signed the Dissent From Darwin statement to boot), to convene an e-mail discussion group that became what is now known as the Altenberg 16.

Science writer Susan Mazur reported on that meeting, and later wrote an entire book about the 16 scientists who were basically affirming what we'd been saying here at ENV for years -- Darwinian evolution is dead. She wrote:

What it amounts to is a gathering of 16 biologists and philosophers of rock star stature – let's call them "the Altenberg 16" – who recognize that the theory of evolution which most practicing biologists accept and which is taught in classrooms today, is inadequate in explaining our existence. It's pre the discovery of DNA, lacks a theory for body form and does not accommodate "other" new phenomena.

When I called Fodor to discuss his article, he joked that he was now in the Witness Protection Program because he'd been so besieged following the LRB piece. ... Fodor also told me that "you can't put this stuff in the press because it's an attack on the theory of natural selection" and besides "99.99% of the population have no idea what the theory of natural selection is".

Since these doubts aren't anything new to many scientists who've been saying this for years, I thought I'd ask them what their initial thoughts about this book are. Here are a few responses.

On his website David Berlinski, author of The Deniable Darwin writes in part:

What is encouraging about Jerry Fodor's and Massimo Piattelli-Palmarini's arguments in What Darwin Got Wrong is just that Fodor and Piattelli- Palmarini had the nerve to make them. What is discouraging about their arguments is just that it has taken them so long to acquire their nerve. Where have you been fellahs?

Every argument that they advance others have advanced before them. Who in particular? Me, for sure. I have called attention to the striking analogy between Skinner and Darwin for more than fifteen years now.

Darwinian propagandists would like the public to believe that there is no scientific debate about the adequacy of evolutionary theory--though scientists have actually been debating it ever since The Origin of Species was published in 1859. Jerry Fodor and Massimo Piattelli-Palmarini's book, What Darwin Got Wrong, is the latest contribution to this long-standing scientific controversy.

Darwin considered natural selection--survival of the fittest--to be the "most important" mechanism of evolution, but Fodor and Piattelli-Palmarini (like many scientist before them) argue that it is not. Although they accept Darwin's idea that living things are descended from a common ancestor, Fodor and Piattelli-Palmarini cite abundant evidence against natural selection.

They call much of the "vast literature" on this subject "distressingly uncritical" and write "it is high time that Darwinists take this evidence seriously."

So the scientific debate continues--the debate that Darwinian propagandists say doesn't exist.

The smoke from Darwin’s 200 birthday candles had barely dissipated when Jerry Fodor and Massimo Piattelli-Palmarini announce “What Darwin Got Wrong” — evolution’s mechanism. Natural selection just can’t cut the mustard, they explain. But since the proposal of a natural mechanism for evolution is the very reason for Darwin’s scientific and cultural importance, his achievement apparently has been way overblown by pretty much the entire biological community. Now, I wonder who else has been saying that for the last few decades?

Fodor correctly understands that natural selection, Darwin's designer substitute mechanism, lacks the creative power that has long been attributed to it. Natural selection by definition only "selects" or favors functional advantage. What we have learned in biology over the last 50 years shows that at every level in the biological hierarchy -- whether we are talking about novel genes, proteins, molecular machines, signal transduction circuits, organs, or body plans -- functional advantage depends upon the occurrence of a series of vastly improbable and tightly coordinated mutational events. Careful quantitative analysis has shown that these events that are so improbable as to put thresholds of selectable function well beyond the reach of chance. The selection and mutation mechanism does not work because the mechanism of natural selection depends on too many improbable things going right before there is anything to select at all.

Posted by Robert Crowther at 1:24 AM | Permalink | TrackBacks (0)

Life arose without design or direction from any intelligent agent. Would you believe it did so in a sun-warmed ocean surface? No? Would you believe an earth-heated vent at the bottom of the same ocean? Would you believe an office microwave that hasn’t been cleaned since the Bush Administration?

The past week’s startling news of backpedaling from the “primordial soup” theory rang a bell, though I wasn’t instantly able to say whose comedy routine it put me in mind of. Hm, was it Monty Python? ScienceDaily carries the story:

For 80 years it has been accepted that early life began in a “primordial soup” of organic molecules before evolving out of the oceans millions of years later. Today the “soup” theory has been overturned in a pioneering paper in BioEssays which claims it was the Earth's chemical energy, from hydrothermal vents on the ocean floor, which kick-started early life.

"Textbooks have it that life arose from organic soup and that the first cells grew by fermenting these organics to generate energy in the form of ATP. We provide a new perspective on why that old and familiar view won't work at all," said team leader Dr Nick lane from University College London. "We present the alternative that life arose from gases (H₂, CO₂, N₂, and H₂S) and that the energy for first life came from harnessing geochemical gradients created by mother Earth at a special kind of deep-sea hydrothermal vent -- one that is riddled with tiny interconnected compartments or pores."

In Signature in the Cell, Stephen Meyer writes about how back in 1985 he came across Thaxton, Bradley and Olson’s The Mystery of Life’s Origin, which “provided a comprehensive critique of the attempts that had been made to explain how the first life had arisen from the primordial ocean, the so-called pre-biotic soup.”

The soup-spilling team writing in BioEssays concentrates on the source of energy needed to power life into existence. Was it from UV radiation, as J.B.S. Haldane theorized in 1929? Or from a hydrothermal vent? This overlooks a much trickier problem: the source not of the relevant energy but the relevant biological information. As Meyer remarks in Signature, origin-of-life scenarios that “just transfer the information problem into the chemical soup itself” fit into a “clear pattern. Every attempt to explain the origin of biological information either failed because it transferred the problem elsewhere or ‘succeeded’ only by presupposing unexplained sources of information.”

Anyway, the lame retreat from a stance previously thumped with tremendous vigor sounds Pythonesque but no, a quick Internet search reveals it’s actually from Get Smart. Along with “Missed it by that much” and “Sorry about that, Chief,” “Would you believe…” was a repeated line from the classic 1960s TV show. It always introduced Agent Maxwell Smart’s attempt to climb down from an earlier, bolder claim in favor of increasingly pitiable ones: “I happen to be an expert in karate, Judo and tempura. Would you believe that I can break eight boards with one karate chop? No? Would you believe three boards? Would you believe a loaf of bread?”

But enough nostalgia. Read the ScienceDaily article here.

Posted by David Klinghoffer at 3:01 PM | Permalink | TrackBacks (0)

A popular Darwinian meme is that humans and chimp genomes are ninety-something percent identical. It varies a bit, but usually hovers close to 99%. The meme hides all sorts of assumptions, of course, but the take home lesson for the headline reader is plain enough: we’re almost exactly the same as chimps.

Though the 99% number has received some qualifiers, and has even been referred to as a “myth” in Science, the basic idea remains firmly entrenched in the media collective consciousness.

But evidence seems to be piling up that the similarities are not nearly what has been advertised. Geneticist Richard Buggs has reflected on this, and has even predicted “that when we have a reliable, complete chimpanzee genome, the overall similarity of the human genome will prove to be close to 70% (and very far from 99%).”

It will be interesting to see how Buggs' prediction holds up over time. If he’s right, this will be one more switch from “meme” to “myth” in the Darwinian ledger.

I should confess that I haven’t followed this debate closely, simply because I don’t think that the meme, even if true, really shows much. Here’s what I mean. Some years ago, a reporter called the Discovery Institute asking for a comment on a new study showing a 75% genetic similarity between human beings and a nematode (if I remember correctly). The reporter asked me what I thought about the discovery that we were 75% identical to a nematode. I suggested that there was a difference between our genomes being quite similar to the nematode’s, and human beings being quite similar to nematodes. That didn’t seem to connect, so I said: “Well, why doesn’t the story cause you to reassess the assumption that we’re basically identical with our DNA? If somebody told me we were 100% chemically identical with chimps, I would conclude that we must be a lot more than mere chemicals, since chimps and humans are quite different. Now since humans and nematodes are obviously quite different, while our genomes are similar, doesn’t that suggest that genetics tells us less about ourselves than we had assumed?” I'm pretty sure my comments didn’t make the story.

Posted by Jay Richards at 8:23 AM | Permalink | TrackBacks (0)

If that dictum looks like a bumper sticker, I apologize — but it’s true all the same. Most of the philosophy of science can be captured by a handful of bumper stickers. Anyway, keep the dictum in mind. In this second installment of the “Seeing Ghosts in the Bushes” blog series — part 1 is here — we’ll ask how the theory of common descent could be tested by fossils. The principle of “what evidence cannot question, evidence cannot support” will be our main guide.

1. Hey, Common Descent Never Pays When She Runs a Stop Sign

Recall that Richard Dawkins argued common descent would be overturned if fossils occurred out of evolutionary sequence. “Evolution could so easily be disproved,” he writes (2009, p. 147), “if just a single fossil turned up in the wrong date order.” This prediction follows a long tradition in evolutionary reasoning, reaching back to the early 20th century, in which the possibility of “Precambrian rabbits” has been regarded as a crucial test of the theory of common descent.

But, as I’ll explain below, “Precambrian rabbits” are found all the time. These fossil discoveries aren’t seen as telling against common descent, however, because the “incompleteness of the fossil record” absorbs the blow. In part 1, for example, I showed how the concept of “ghost lineages” allows evolutionary theorists to accommodate anomalous stratigraphic (fossil) distributions. In short, when fossils occur out of order — as either too early or too late — ghost lineages mend the damage by invisibly extending the temporal ranges of groups, well beyond the actual fossil data, to achieve congruence with expectations. In part 2, I’ll show how common descent is further insulated from paleontological challenges by a protective buffer of auxiliary hypotheses.

Think about the problem this way. When a prediction of common descent fails, who pays for the failed prediction?

The cop writes a ticket for the broken prediction and hands it through the window. The vehicle belongs to common descent (CD), and indeed, she was driving when it was pulled over. Nevertheless, CD passes the ticket to one of her passengers.

“Take care of this for me, won’t you?" she says, as she sips her imported bottled water.

You get the picture. Common descent never pays for a ticket, because everyone else picks up the cost.

Let’s start with an influential paper by two leading paleontologists, from the early 1990s.

2. Norell and Novacek 1992: How Well Does the Fossil Record Match Cladistic Predictions?

In 1992, vertebrate paleontologist Mark Norell — who coined the term “ghost lineage” — and his American Museum of Natural History colleague Michael Novacek, asked an important question: How well does the fossil record fit with evolutionary expectations based on cladistic analysis? (A cladistic analysis of fossil and extant groups uses their characters to derive a cladogram, an evolutionary tree predicted independently of the groups’ stratigraphic [geological] position.) As Norell and Novacek explain,

Our purpose was to examine the reliability of the fossil record in recovering the sequence of fossil divergence events. The cladistic result [prediction] is not necessarily the closer match to the “true” phylogeny; it simply provides an independent means of assessing the timing of evolutionary events in the fossil record. (1992, p. 1691)

To assess the congruence of cladograms and fossils, Norell and Novacek assigned ranks to each. See Figure 1, from their paper: “Age rank” gives the location in geological time of the fossil distributions of groups ABCD, whereas “clade rank” gives the branching or phylogenetic order of the same groups, based in this case not on stratigraphy, but on the anatomical (or molecular) characters of ABCD.

Fig. 1. Norell and Novacek (1992, p. 1692) assigned ranks to vertebrate groups, using both stratigraphic distribution and cladistic branching order. These diagrams show the ranks for hypothetical groups ABCD.

When plotted in this way, the two ranks — if congruent for any group — should produce points lying along a diagonal. "Complete congruence between the fossil record and the cladogram," write Norell and Novacek, "in sequence of ranks and level of precision will produce a diagonal line of points intersecting the axes at their origin" (1992, p. 1691; emphasis added). See Figure 2, where the blue diagonal represents congruence. Points falling above that line mark groups arising too early in the fossil record, with respect to their clade rank, whereas points below the diagonal represent groups arising too late.

Fig. 2. For any taxonomic group, congruence between its age (fossil) rank and clade rank will produce a point lying on the blue diagonal. Points above that line represent groups that appear too early in the fossil record, with respect to their clade rank, whereas points below represent groups appearing too late in the fossil record with respect to clade rank.

Norell and Novacek then plotted age and clade ranks for several vertebrate groups. Figure 3 shows two such plots from their paper, for equids (i.e., horses and their relatives) and higher primates.

Fig. 3. Plots of age ranks as a function of clade ranks for two mammalian groups, equids and higher primates. The "pretty" plot for equids shows most of the points falling close to the diagonal, indicating (relatively) good congruence. The "not so pretty" plot for higher primates, by contrast, shows considerable scatter. For instance, the taxon marked by the green arrow appears too early in the fossil record, whereas the taxon marked by the red arrow appears too late.

Note that the equid plot corresponds well to the congruence diagonal, with only a couple of points straying. Norell and Novacek call this a "remarkable match of that [fossil] record with cladistic results" (1992, p. 1692). The higher primate plot, on the other hand, is frankly a mess. The taxon indicated by the green arrow, for instance, appears too early in the record, whereas the taxon marked by the red arrow appears very late (in both cases, with respect to cladistic predictions).

Now, before we look at how Norell and Novacek explained departures from theoretical expectation — including the not-so-pretty scatter in the higher primate plot — time for another visit with the logic of testing. We've got a handy bumper sticker for that.

3. When Data Don't Cooperate

Testing a theory does not mean applauding whenever data and theory agree, while waving away or ignoring the instances where they don't. That would be like assessing someone's driving record by counting only the days when she didn't speed or run through stop signs. Here's another bumper sticker to make the point:

Remember the question motivating all this: How can common descent be challenged or questioned by paleontological evidence? Dawkins, following Julian Huxley, J.B.S. Haldane, and many other evolutionists, argues that common descent would be falsified if fossils were found out of evolutionary sequence.

This prediction may be represented schematically as follows (see Figure 4):

Fig. 4. Common Descent (CD) is widely said to predict that fossils should occur in the geological column in the correct evolutionary order.

If the prediction of "fossils in correct evolutionary order" follows from common descent, then when the prediction is overturned — as in the case of higher primate fossils (see the not-so-pretty plot, in Fig. 3, above) — common descent is falsified, at least for that group.

Right?

4. Don't Be So Naïve, Paul

Of course not. Figure 5 shows what actually happens:

Fig. 5. When the prediction from CD of correct fossil order fails, the auxiliary hypothesis of "poor fossil record" absorbs the anomaly. CD is thereby protected from observational challenge.

Thus, when Norell and Novacek assessed the lack of congruence in the higher primate plot, guess who paid the ticket? Hint — not the driver:

The relationships examined here also reveal that the quality of the fossil record judged from other perspectives does not necessarily reveal its match with independently derived phylogenetic evidence....the primate fossil record poorly reflects higher level cladistic branching patterns. This is because some taxa (tarsiers and cheirogalines, for instance) thought to have branched off very early in primate history appear late in the record or have no fossil record. (1992, p. 1692; emphasis added)

Well, go figure. The higher primate fossil record is unreliable. Common descent is still true, of course. (In part 3 of this series, I'll review a new theory for the common descent of the primates that sets their fossil record entirely to one side, as completely unreliable.)

In a deeply insightful paper published in 1978, which deserves to be better known, systematist Gareth Nelson grasped that what he calls "the paleontological argument" — namely, that fossils provide a reliable guide to evolutionary relationships — cannot be tested. Figure 5 shows why: the ad hoc hypothesis of the incompleteness of the fossil record absorbs any contrary evidence. As Nelson (1978, p. 331) writes,

Within the history of paleontology, I am aware of numerous apparent falsifiers of the paleontological argument; these have usually been rendered impotent as falsifiers by the ad hoc alternative that the fossil record was not as complete as previously believed....The paleontological argument seems fallacious because it is accepted in principle as non-falsifiable (it is always protected from falsification by an ad hoc alternative that is always, and obviously, true).

The "ad hoc alternative" is always true, because new fossils are always being found. As Nelson (1978, p. 331) notes — one can almost see him grinning — "The ad hoc alternative admittedly has appeal: how could its truth be doubted with the newly discovered fossils in hand?"

You can't lose betting on the incompleteness of the fossil record. And, because you can't lose, this ad hoc hypothesis works as a perfect sink to absorb any anomalous data the fossil record may reveal. Observe what happened recently with the discovery of the anomalously early Polish trackways. Did anyone question the common descent of the tetrapods?

Whaddya, crazy?

5. But No One Expects Common Descent to Pay for Her Tickets

This may seem a harsh judgment. It isn't. Following the publication of Norell and Novacek 1992, a flurry of research began, led mainly by paleontologist Michael Benton and his co-workers, to examine the congruence of the fossil record and cladograms. I'll discuss their research in greater depth in part 3. Here I want only to look at how Benton et al. handled the lack of congruence they found in one of their studies.

"What Causes Poor Matching of Age and Clade Data?" That's the question Benton et al. asked in their 1999 paper on the problem (Benton, Hitchin and Wills 1999, p. 592). And here is their answer, which I have formatted as a series of bullet points for ease of reference:

Variations in congruence between cladograms and stratigraphic data result from several factors:

1. differences in the quality of cladograms;

2. differences in the quality of the fossil record;

3. stratigraphic problems;

4. categorical (taxonomic) focus; and

5. sampling density.

Only by looking at each case in some detail can we hope to determine the reasons for particularly good or particularly bad matching. (1999, p. 592)

Notice what theory is NOT in the list of possibilities to explain lack of congruence: the falsity of common descent itself. Figure 6 shows the logic. The investigator has (at least) five possible ad hoc or auxiliary hypotheses available to absorb any anomalous paleontological data.

Fig. 6. Multiple possible ad hoc or auxiliary hypotheses are available to explain lack of congruence between the fossil record and cladistic predictions. These may be employed singly or in combination. Common descent (CD) is thus protected from observational challenge.

Common descent, although sitting in the driver's seat, can pass any ticket she receives to one of her passengers. And she will.

Okay, I guess.

But what evidence cannot question, evidence cannot support.

In part 3, we'll look at how all this plays out in current evolutionary research.

References

Benton, Michael, Rebecca Hitchin, and Matthew Wills. 1999. Assessing Congruence Between Cladistic and Stratigraphic Data. Systematic Biology 48:581-596.

Dawkins, Richard. 2009. The Greatest Show on Earth: The Evidence for Evolution. New York: The Free Press.

Nelson, Gareth. 1978. Ontogeny, Phylogeny, Paleontology, and the Biogenetic Law. Systematic Zoology 27:324-345.

Norell, Mark and Novacek, Michael. 1992. The Fossil Record and Evolution: Comparing Cladistic and Paleontologic Evidence for Vertebrate History. Science 255:1690-93.

Posted by Paul Nelson at 10:26 AM | Permalink | TrackBacks (0)

Download the "Truth or Dare" with Dr. Ken Miller Lecture Guide Permission Granted to Copy and Distribute for Educational Use.

The segments of this guide have included:

Science and Religion: Is Evolution “Random and Undirected”?

Misrepresenting the Definition of Intelligent Design

Confusing Evidence for Common Ancestry With Evidence for Darwinian Evolution

The Name-Dropping Approach to Transitional Fossils

Spinning Tales About the Bacterial Flagellum

Misrepresenting Michael Behe’s Arguments for Irreducible Complexity of the Blood Clotting Cascade

Ken Miller and the Evolution of the Immune System: “Not Good Enough”?

The Darwinian educational establishment doesn’t make it easy for you to become objectively informed on the topic of evolution and intelligent design, but with a little work on your own, it can be done. If you want to base your views on a full and complete understanding of the scientific evidence, you will need to pro-actively research and investigate the pro-ID arguments that many of your faculty may be opposing, misrepresenting, or perhaps even outright censoring. Yes, take courses advocating evolution. But also read material from credible Darwin skeptics to learn about other viewpoints. Only then can you truly make up your mind in an informed fashion.

With a little proactive self-education, critical thinking, and patience, you can keep yourself informed in this debate. Many of the websites listed below contain helpful information and resources about evolution and intelligent design.

I hope this guide is helpful and wish you the best as you explore this exciting and challenging debate.

Posted by Casey Luskin at 12:00 AM | Permalink | TrackBacks (0)

Download the full "Truth or Dare with Dr. Ken Miller" Lecture Guide Permission Granted to Copy and Distribute for Educational Use.

In Only a Theory, Miller claims that when the plaintiffs' attorneys at the Dover trial did a literature-dump bluff on Behe during cross-examination—placing before him over 50 papers and nearly a dozen books purportedly explaining the evolution of the immune system—that Behe said that they were "not 'good enough.’" Miller even goes so far as to characterize Behe's response as follows: "Even when presented with every opportunity to make their case, the defenders of design resorted to little more than saying 'It's not good enough for me' in the face of overwhelming evidence for evolution."⁴¹ What did Behe really say?

If by overwhelming evidence for "evolution," Miller meant neo-Darwinian evolution, where random mutation and natural selection are the driving force generating biological complexity in an adaptive, step-by-step fashion, then Behe is on quite firm ground in doubting Miller's assertion of "overwhelming" evidence for the evolution of the immune system. Behe knew this, and thus stated during his cross examination about the immune system: "In many of [the papers] they're not actually discussing mutation. They're discussing similarities and sequences between parts of the immune system in vertebrates and some elements of transposons."⁴²

The plaintiffs’ attorney wouldn’t give up. In another exchange Behe was asked "Now, these articles rebut your assertion that scientific literature has no answers on the origin of the vertebrate immune system?" and he replied:

A. No, they certainly do not. My answer, or my argument is that the literature has no detailed rigorous explanations for how complex biochemical systems could arise by a random mutation and natural selection and these articles do not address that.

Q. So these are not good enough?

A. They're wonderful articles. They're very interesting. They simply just don't address the question that I pose.⁴³

The relentless plaintiffs’ attorney then pestered Behe again with nearly the same question “Is that your position today that these articles aren't good enough, you need to see a step-by-step description?” and Behe clearly replied, “These articles are excellent articles I assume. However, they do not address the question that I am posing. So it's not that they aren't good enough. It's simply that they are addressed to a different subject.”⁴⁴

The plaintiffs’ attorney continued pressing Behe, and later Behe again emphasized this point: “Most of them have evolution or related words in the title, so I can confirm that, but what I strongly doubt is that any of these address the question in a rigorous detailed fashion of how the immune system or irreducibly complex components of it could have arisen by random mutation and natural selection.”⁴⁵

Does Behe say, as Miller characterizes it, "It's not good enough for me," or in Judge Jones' words, the papers are "not 'good enough’”? Not at all, because Behe actually says: "These articles are excellent articles I assume. However, they do not address the question that I am posing. So it's not that they aren't good enough. It's simply that they are addressed to a different subject."

In other words, Behe said precisely the opposite of what Miller claims Behe said. Of course Miller copied the error from Judge Jones, who copied the error from the ACLU's "Findings of Facts and Conclusions of Law" brief,⁴⁶ but unfortunately this false account of Behe’s testimony continues to be perpetuated by Miller in his books and lectures about Dover.

More important than all of this is the fact that Behe’s response to these papers was right on target: the papers dumped on Behe during cross-examination made for a nice display of courtroom theatrics, but they did not establish a step-by-step Darwinian explanation of the origin of the immune system. Instead, the papers made comparisons of DNA sequences—a type of evidence that doesn’t refute irreducible complexity, making the same mistake discussed earlier in, “Confusing Evidence for Common Ancestry with Evidence for Darwinian Evolution.”

References Cited:

[41.] Only a Theory, p. 74 (2008).

[42.] Day 12 PM testimony, p. 12.

[43.] Day 12 PM testimony, p. 16.

[44.] Day 12 PM testimony, pp. 18-19, emphasis added.

[45.] Day 12 PM testimony, pp. 20-21.

[46.] See ”A Comparison of Judge Jones' Opinion in Kitzmiller v. Dover with Plaintiffs' Proposed ‘Findings of Fact and Conclusions of Law’"

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Florida has all the fun. Fresh on the heels of the Signature in the Cell event in Tampa, we have learned from our friends at the C. S. Lewis Society that Discovery Senior Fellow David Berlinski will be speaking at a couple events this week, including "The Deniable Darwin: Has Science Buried Religion?" this Thursday, Feb 4th at 3:30 pm. The presentation will take place at Florida International University's Graham Center Room 140.

Following that, there will be Darwin vs. Design "Pizza Bash" featuring Dr. Berlinski and Dr. Tom Woodward this Saturday:

Pizza Kick-off: On Saturday, Feb 6th at 6:00 pm, at the First Alliance Church of Ft. Lauderdale (900 SW 31st Ave.) Dr. Tom Woodward and the C. S. Lewis Society are hosting a pizza-bash "meet and greet Berlinski/Woodward" for interested persons in the Ft. Lauderdale area and beyond. There is no charge; there will be a basket for free-will donations. RSVP is requested; email twdwrd@tampabay.rr.com to list name, phone and number of group coming.

Main Course at 7:00 pm: Dr. Woodward will give a powerpoint overview of the current Darwin-vs-Design clash. Then he will introduce and interview Dr. David Berlinski about the flaws that he sees in Darwinian theory and in the preachings of the "New Atheists" such as Richard Dawkins. Dr. Berlinski, self-described as a secular Jew, has emerged as one of the world's most powerful critics of Darwinian theory. His sizzling critique of the New Atheism, The Devil's Delusion, along with the newly released The Deniable Darwin, have caused a buzz about his startling insights.

For more information, contact Dr. Tom Woodward, Director of C. S. Lewis Society, at 727-642-8574 or twdwrd@tampabay.rr.com.

Posted by Anika Smith at 9:55 AM | Permalink | TrackBacks (0)