|Links to our 8-Part Series, “The NCSE, Judge Jones, and Citation Bluffs About the Origin of New Functional Genetic Information”:
• Part 1: Judge Jones’s Misguided NCSE-Scripted Kitzmiller Ruling and the Origin of New Functional Genetic Information
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:
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
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.
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.
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.
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.
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.
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.
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.
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.
[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).
[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).
[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).
[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).