21. Ohno, “The Notion of the Cambrian Pananimalia Genome.”
22. Dembski, The Design Inference, 175–223. Dembski often uses the figure 1 in 10150 as his universal probability bound, but this figure derives from Dembski rounding up the exponent in the figure that he actually calculates. See my discussion of the derivation of Dembski’s universal probability bound in Signature in the Cell, Chapter 10.
23. Dawkins, The Blind Watchmaker, 139.
Chapter 11: Assume a Gene
1. Stephen C. Meyer, “The Origin of Biological Information and the Higher Taxonomic Categories.”
2. For detailed discussions of facts of the Sternberg case, see “Smithsonian Controversy,” www.richardsternberg.com/smithsonian.php; U.S. Office of Special Counsel Letter (2005) at www.discovery.org/f/1488; United States House of Representatives Committee on Government Reform, Subcommittee Staff Report, “Intolerance and the Politicization of Science at the Smithsonian” (December 2006), at www.discovery.org/f/1489; Appendix, United States House of Representatives Committee on Government Reform, Subcommittee Staff Report (December 2006) at www.discovery.org/f/1490.
3. See Holden, “Defying Darwin”; Giles, “Peer-Reviewed Paper Defends Theory of Intelligent Design,” 114; Agres, “Smithsonian ‘Discriminated ’Against Scientist”; Stokes, “ … And Smithsonian Has ID Troubles”; Monastersky, “Society Disowns Paper Attacking Darwinism.”
4. Powell, “Controversial Editor Backed”; Klinghoffer, “The Branding of a Heretic.”
5. Hagerty, “Intelligent Design and Academic Freedom.
6. See www.talkreason.org/AboutUs.cfm.
7. Gishlick, Matzke, and Elsberry, “Meyer’s Hopeless Monster,” www.talkreason.org/AboutUs.cfm.
8. Jones, Kitzmiller et al. v. Dover Area School District.
9. Matzke and Gross, “Analyzing Critical Analysis,” 42.
10. Matzke and Gross, “Analyzing Critical Analysis,” 42.
11. Matzke and Gross, “Analyzing Critical Analysis,” 42.
12. See Chapter 10, n. 15, for the four major mechanisms by which DNA is duplicated.
13. For example, see Zhen et al., “Parallel Molecular Evolution in an Herbivore Community”; Li et al., “The Hearing Gene Prestin Unites Echolocating Bats and Whales”; Jones, “Molecular Evolution”; Christin, Weinreich, and Bresnard, “Causes and Evolutionary Significance of Genetic Convergence”; Rokas and Carroll, “Frequent and Widespread Parallel Evolution of Protein Sequences.” According to Dávalos and colleagues, “In-depth analyses of specific genes in the context of multilocus phylogenies have also shown that adaptive evolution leading to convergence, once thought to be extremely rare, is as much a source of conflict among gene trees as it is between morphological and molecular phylogenies” (“Understanding Phylogenetic Incongruence,” 993).
14. Shen et al., “Parallel Evolution of Auditory Genes for Echolocation in Bats and Toothed Whales”; Li et al., “The Hearing Gene Prestin Unites Echolocating Bats and Whales”; Jones, “Molecular Evolution.”
15. Khalturin et al., “More Than Just Orphans”; Merhej and Raoult, “Rhizome of Life, Catastrophes, Sequence Exchanges, Gene Creations, and Giant Viruses”; Beiko, “Telling the Whole Story in a 10,000-Genome World.”
16. Suen et al., “The Genome Sequence of the Leaf-Cutter Ant Atta cephalotes Reveals Insights into Its Obligate Symbiotic Lifestyle” (“We also found 9,361 proteins that are unique to A. cephalotes, representing over half of its predicted proteome,” 5). See also Smith et al., “Draft Genome of the Globally Widespread and Invasive Argentine Ant (Linepithema humile)” (“A total of 7,184 genes (45%) were unique to L. humile relative to these three other species,” 2).
17. Tautz and Domazet-Lošo, “The Evolutionary Origin of Orphan Genes”; Beiko, “Telling the Whole Story in a 10,000-Genome World”; Merhej and Raoult, “Rhizome of Life, Catastrophes, Sequence Exchanges, Gene Creations, and Giant Viruses.”
18. Lyell, Principles of Geology.
19. See Pray and Zhaurova, “Barbara McClintock and the Discovery of Jumping Genes (Transposons).”
20. Long et al., “The Origin of New Genes,” 867.
21. Nurminsky et al., “Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila,” 574.
22. Chen, DeVries, and Cheng, “Evolution of Antifreeze Glycoprotein Gene from a Trypsinogen Gene in Antarctic Notothenioid Fish,” 3816.
23. Courseaux and Nahon, “Birth of Two Chimeric Genes in the Hominidae Lineage.”
24. Knowles and McLysaght, “Recent de Novo Origin of Human Protein-Coding Genes.”
25. Wu, Irwin, and Zhang, “De Novo Origin of Human Protein-Coding Genes.”
26. Guerzoni and McLysaght, “De Novo Origins of Human Genes”; see also Wu, Irwin, and Zhang, “De Novo Origin of Human Protein-Coding Genes.”
27. Siepel, “Darwinian Alchemy.”
28. Siepel, “Darwinian Alchemy.”
29. Siepel, “Darwinian Alchemy.”
30. As Siepel notes, “These apparent de novo gene origins raise the question of how evolution by natural selection can produce functional genes from noncoding DNA. While a single gene is not as complex as a complete organ, such as an eye or even a feather, it still has a series of nontrivial requirements for functionality, for instance, an ORF [an open reading frame], an encoded protein that serves some useful purpose, a promoter capable of initiating transcription, and presence in a region of open chromatin structure that permits transcription to occur. How could all of these pieces fall into place through the random processes of mutation, recombination, and neutral drift … ?” (“Darwinian Alchemy”).
31. Of course, one could argue that the mutational processes that Long invokes to explain the origin of new genes from preexisting cassettes of genetic information themselves explain the origin of the information in those cassettes in the first place. This view would suggest that the scenarios that Long cites do not so much beg the question as much as generate a regress of explanation terminating with the ultimate origin of biological information at the point of the origin of the first life. This view implies that, although the ultimate origin of biological information and the closely associated question of life’s first origin may remain a mystery, the processes that Long cites account for all subsequent informational increases during the course of biological evolution. But this view still does not explain how shuffling preexisting cassettes of information generates the specific arrangements of the characters that make up those cassettes.
32. Zhang, Zhang, and Rosenberg, “Adaptive Evolution of a Duplicated Pancreatic Ribonuclease Gene in a Leaf-Eating Monkey.” The genes that code for these two proteins differ by 12 nucleotides in their coding sequences. Those nucleotide differences produce two proteins that differ from each other in their overall electronegativity. This difference, in turn, allows the protein RNASE1B to operate at a slightly lower pH than the other protein, RNASE1. Since other primates have only the RNASE1 protein, Zhang, Zhang, and Rosenberg hypothesize that the evolution of this second gene and protein gave individuals within the species of monkey a selective advantage. To explain the origin of the second gene, they posit a common ancestral gene, a gene duplication event, and the accumulation of different mutations on the duplicate copy (the RNASE1B) over time.
33. In this study (“Adaptive Evolution of Cid, a Centromere-Specific Histone in Drosophila”), Malik and Henikoff infer that “adaptive evolution has occurred on both the D. melanogaster and D. simulans lineages since their split from a common ancestor.” They base this inference on an analysis of the ratio of “synonymous” and “nonsynonymous” mutations in the genomes of these organisms. The study found that many of the differences/mutations in nucleotide base sequences changed amino-acid sequence (called “nonsynonymous” mutations), while some did not (called synonymous, or “silent,” mutations). A higher percentage of these differences changed the amino-acid sequence than would be expected from neutral evolution alone, leading the authors to infer that “adaptive evolutio
n has occurred on both the D. melanogaster and D. simulans lineages since their split from a common ancestor.” Since some of these differences exist in the region of the protein that binds to the chromosome, they may have affected the protein’s functional binding ability. But the authors of the paper identify no specific functional effects of these amino-acid differences and base their claim of “strong evidence for the adaptive evolution of Cid” solely upon comparisons of the relative numbers of a handful of synonymous and nonsynonymous differences between the genes.
34. Enard et al., “Molecular Evolution of FOXP2, a Gene Involved in Speech and Language”; Zhang, Webb, and Podlaha, “Accelerated Protein Evolution and Origins of Human-Specific Features.”
35. Enard et al., “Molecular Evolution of FOXP2, a Gene Involved in Speech and Language.”
36. Long et al., “The Origin of New Genes,” 866.
37. Darnell and Doolittle, “Speculations on the Early Course of Evolution”; Hall, Liu, and Shub, “Exon Shuffling by Recombination Between Self-Splicing Introns of Bacteriophage T4”; Rogers, “Split-Gene Evolution”; Gilbert, “The Exon Theory of Genes”; Doolittle et al., “Relationships of Human Protein Sequences to Those of Other Organisms.”
38. For example, Arli A. Parikesit and colleagues note that “Although there is a statistically significant correlation between protein domain boundaries and exon boundaries, about two thirds of the annotated protein domains are interrupted by at least one intron, and on average a domain contains 3 or 4 introns” (“Quantitative Comparison of Genomic-Wide Protein Domain Distributions,” 96–97; internal citations omitted).
39. Gauger, “Why Proteins Aren’t Easily Recombined.”
40. Axe, “The Limits of Complex Adaptation.” See also Voigt et al., “Protein Building Blocks Preserved by Recombination.”
41. Experimental shuffling of genes has proven fruitful only when the parent genes are highly similar. See He, Friedman, and Bailey-Kellogg, “Algorithms for Optimizing Cross-Overs in DNA Shuffling.”
42. In 2012, a research group at the University of Washington reported success in designing a few stable protein folds using a few rules, a lot of computational analysis, and trial and error (only 10 percent of the designed proteins folded as predicted). Though these proteins did form stable folds, they did not perform any actual biological function. The researchers acknowledge that there is likely a tradeoff between stability and functionality in natural proteins. It remains to be seen whether these methods of sequence engineering can create new, stable folds capable of enzymatic activity. What this research highlights is the extreme difficulty of intelligently designing a stable and functional protein from scratch, even with the best minds and computational resources working on the problem. There is, therefore, little reason to think that unguided process of exon shuffling could generate both a stable and functional protein. See Nobuyasu et al., “Principles for Designing Ideal Protein Structures”; Marshall, “Proteins Made to Order.”
43. Altamirano et al., “Directed Evolution of New Catalytic Activity Using the Alpha/Beta-Barrel Scaffold.” See also Altamirano et al., “Retraction: Directed Evolution of New Catalytic Activity Using the Alpha/Beta-Barrel Scaffold.”
44. Gauger, “Why Proteins Aren’t Easily Recombined.”
45. Axe, “The Case Against Darwinian Origin of Protein Folds.”
46. See, e.g., Long and Langley, “Natural Selection and the Origin of Jingwei, a Chimeric Processed Functional Gene in Drosophila”; Wang et al., “Origin of Sphinx, a Young Chimeric RNA Gene in Drosophila melanogaster”; Begun, “Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila.”
47. Long et al., “Exon Shuffling and the Origin of the Mitochondrial Targeting Function in Plant Cytochrome cl Precursor.”
48. Long et al., “The Origin of New Genes. See also Begun, “Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila.”
49. Nurminsky et al., “Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila.”
50. Nurminsky et al., “Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila.”
51. Brosius, “The Contribution of RNAs and Retroposition to Evolutionary Novelties.”
52. Begun, “Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila.”
53. Begun, “Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila.”
54. Papers cited by Long where natural selection was invoked even though the function of the gene and thus the function being selected for was unknown include Begun, “Origin and Evolution of a New Gene Descended from Alcohol Dehydrogenase in Drosophila”; Long and Langley, “Natural Selection and the Origin of Jingwei, a Chimeric Processed Functional Gene in Drosophila”; and Johnson et al., “Positive Selection of a Gene Family During the Emergence of Humans and African Apes.”
55. Logsdon and Doolittle, “Origin of Antifreeze Protein Genes.”
56. Courseaux and Nahon, “Birth of Two Chimeric Genes in the Hominidae Lineage.”
57. Paulding, Ruvolo, and Haber, “The Tre2 (USP6) Oncogene Is a Hominoid-Specific Gene.”
58. Chen, DeVries, and Cheng, “Convergent Evolution of Antifreeze Glycoproteins in Antarctic Notothenioid Fish and Arctic Cod.”
59. Logsdon and Doolittle, “Origin of Antifreeze Protein Genes.”
60. Johnson et al., “Positive Selection of a Gene Family During the Emergence of Humans and African Apes.”
61. See Nurminsky et al., “Selective Sweep of a Newly Evolved Sperm-Specific Gene in Drosophila”; Chen, DeVries, and Cheng, “Evolution of Antifreeze Glycoprotein Gene from a Trypsinogen Gene in Antarctic Notothenioid Fish”; Courseaux and Nahon, “Birth of Two Chimeric Genes in the Hominidae Lineage”; Knowles and McLysaght, “Recent de Novo Origin of Human Protein-Coding Genes”; Wu, Irwin, and Zhang, “De Novo Origin of Human Protein-Coding Genes”; Siepel, “Darwinian Alchemy.”
Chapter 12: Complex Adaptations and the Neo-Darwinian Math
1. Frazzetta, “From Hopeful Monsters to Bolyerine Snakes?” 62–63.
2. Frazzetta, “From Hopeful Monsters to Bolyerine Snakes?” 63.
3. Gould, “Return of the Hopeful Monsters,” 28.
4. Frazzetta, “From Hopeful Monsters to Bolyerine Snakes?” 63.
5. Frazzetta, Complex Adaptations in Evolving Populations, 20.
6. As Darwin wrote in the Origin, “If we must compare the eye to an optical instrument, we ought in imagination to take a thick layer of transparent tissue, with a nerve sensitive to light beneath, and then suppose every part of this layer to be continually changing slowly in density, so as to separate into layers of different densities and thicknesses, placed at different distances from each other, and with the surfaces of each layer slowly changing in form” (188–89).
7. Frazzetta, Complex Adaptations in Evolving Populations, 21.
8. Frazzetta, “Modeling Complex Morphological Change in Evolution,” 129.
9. Frazzetta, “Modeling Complex Morphological Change in Evolution,” 130.
10. Ehrlich and Holm, The Process of Evolution, 157.
11. Until a famous experiment performed by Oswald Avery of the Rockefeller Institute in 1944, many biologists still suspected that proteins might actually be the repositories of genetic information. Meyer, Signature in the Cell, 66. Avery, MacCleod, and McCarty, “Induction of Transformation by a Deoxyribonucleic Acid Fraction Isolated from Pneumococcus Type III.”
12. Bateson, “Heredity and Variation in Modern Lights,” 83–84.
13. Withgott, “John Maynard Smith Dies.”
14. Salisbury, “Natural Selection and the Complexity of the Gene,” 342–43.
15. Maynard Smith, “Natural Selection and the Concept of a Protein Space,” 564.
16. As Maynard Smith writes in Nature: “If evolution by natural selection is to occur, functional proteins must form a continuous network which can be traversed by unit mutati
onal steps without passing through nonfunctional intermediates” (“Natural Selection and the Concept of a Protein Space,” 564).
17. Maynard Smith, “Natural Selection and the Concept of a Protein Space,” 564, emphasis added.
18. Maynard Smith, “Natural Selection and the Concept of a Protein Space,” 564.
19. Orr, “The Genetic Theory of Adaptation,” 123.
20. Behe and Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues.”
21. Wen-Hsiung, Molecular Evolution, 427
22. Wen-Hsiung, Molecular Evolution, 427.
23. Behe, The Edge of Evolution, 54.
24. “Powerball—Prizes and Odds,” Powerball, http://www.powerball.com/powerball/pb_prizes.asp.
25. “Powerball—Prizes and Odds,” Powerball, http://www.powerball.com/powerball/pb_prizes.asp.
26. Behe and Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” 2661.
27. Lynch and Conery, “The Origins of Genome Complexity,” 1401–02.
28. Behe and Snoke, “Simulating Evolution by Gene Duplication of Protein Features That Require Multiple Amino Acid Residues,” 2661.
29. For the purpose of Behe’s argument it did not matter whether the mutations involved in a single CCC trait arose in a stepwise, or coordinated fashion. Behe was not calculating how long it would take for a single CCC trait to arise. That chloroquine resistance only arises once in every 1020 malarial cells was an observed empirical fact based upon public health studies, not a calculation of waiting times based upon a population genetics model. [See White, “Antimalarial Drug Resistance,” 1085.] What Behe was calculating was how long it would take for a hypothetical trait to arise that did require two coordinated mutations, each of the complexity of a single CCC, in order to function—what he called a “double CCC.” Whether or not generating a single CCC itself required coordinated mutations was irrelevant. This aspect of his argument has been largely misunderstood by his critics. [See Miller, “Falling Over the Edge,” 1055–56; Gross, “Design for Living,” 73; Coyne, “The Great Mutator (Review of The Edge of Evolution, by Michael J. Behe),” 40–42; Nicholas J. Matzke, “The Edge of Creationism,” 566–67.] It’s worth noting that although Behe’s calculation was for a hypothetical trait, he went on to argue on independent biological grounds that “life is bursting” (63) with features that would require a double CCC to arise.
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