30. Behe, The Edge of Evolution, 135.
31. This assumes that every one of these organisms would be under selection for that particular trait—a completely unrealistic assumption.
32. Durrett and Schmidt, “Waiting for Two Mutations,” 1507.
33. Behe, The Edge of Evolution, 84–102.
34. Gauger and Axe, “The Evolutionary Accessibility of New Enzyme Functions: A Case Study from the Biotin Pathway.”
35. Gauger et al., “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness”; Durrett and Schmidt, “Waiting for Two Mutations.”
Chapter 13: The Origin of Body Plans
1. Nüsslein-Volhard and Wieschaus, “Mutations Affecting Segment Number and Polarity”; Wieschaus, “From Molecular Patterns to Morphogenesis.” As he comments: “If transcription of a gene was essential for embryonic development, homozygous embryos [i.e., those missing both copies of the gene] should develop abnormally when that gene was eliminated… . Based on these defects, it should be possible to reconstruct the normal role of each gene” (316).
2. St. Johnston, “The Art and Design of Genetic Screens,” 177.
3. Quotes recorded in contemporaneous notes taken by philosopher of biology Paul Nelson, who was in attendance at this lecture.
4. Quotes recorded in contemporaneous notes taken by philosopher of biology Paul Nelson, who was in attendance at this lecture.
5. Arthur, The Origin of Animal Body Plans, 21; Cameron et al., “Evolution of the Chordate Body Plan: New Insights from Phylogenetic Analyses of Deuterostome Phyla”; Michael, “Arthropods: Developmental Diversity Within a (Super) Phylum”; Peterson and Davidson, “Regulatory Evolution and the Origin of the Bilaterians”; Carroll, “Endless Forms: The Evolution of Gene Regulation and Morphological Diversity”; Halder et al., “Induction of Ectopic Eyes by Targeted Expression of the Eyeless Gene in Drosophila.”
6. Arthur, The Origin of Animal Body Plans, 21.
7. Van Valen, “How Do Major Evolutionary Changes Occur?” 173.
8. Thomson, “Macroevolution,” 111.
9. John and Miklos, The Eukaryote Genome in Development and Evolution, 309.
10. Thomson, “Macroevolution.”
11. See, e.g., the special issue of Development (December 1996) dedicated to the large-scale mutagenesis of the model vertebrate Danio rerio (the zebrafish), especially Haffter et al., “The Identification of Genes with Unique and Essential Functions in the Development of the Zebrafish, Danio rerio”; or the many fruitfly mutagenesis experiments summarized in Bate and Arias, eds., The Development of Drosophila melanogaster. Summarizing the evidence from a wide range of animal systems, Wallace Arthur writes, “Those genes that control key early developmental processes are involved in the establishment of the basic body plan. Mutations in these genes will usually be extremely disadvantageous, and it is conceivable that they are always so” (The Origin of Animal Body Plans, 14, emphasis in original). Arthur goes on to speculate that because developmental regulatory genes often differ between phyla, perhaps “mutations of these genes are sometimes advantageous” (15). He offers no evidence for such mutations, however, other than as a deduction from his prior assumption of common descent.
12. Fisher, The Genetical Theory of Natural Selection, 44.
13. Wallace, “Adaptation, Neo-Darwinian Tautology, and Population Fitness,” 70.
14. Nüsslein-Volhard and Wieschaus, “Mutations Affecting Segment Number and Polarity in Drosophila”; Lawrence and Struhl, “Morphogens, Compartments and Pattern.”
15. Van Valen, “How Do Major Evolutionary Changes Occur?” 173.
16. McDonald, “The Molecular Basis of Adaptation,” 93.
17. McDonald, “The Molecular Basis of Adaptation,” 93.
18. Wimsatt, “Generativity, Entrenchment, Evolution, and Innateness: Philosophy, Evolutionary Biology, and Conceptual Foundations of Science”; Wimsatt and Schank, “Generative Entrenchment, Modularity and Evolvability: When Genic Selection Meets the Whole Organism.”
19. Nelson notes that there is one noteworthy exception to this generalization: the loss of structures. A wide range of well-documented cases—including cave animals, island birds and insects, and marine and freshwater fishes—show that many animals will tolerate, or actually thrive, after losing traits to mutation—as long as those traits are not essential for survival in some specialized environment. For example, macromutations resulting in loss of vision have had no deleterious effects on some species of now blind cave fish that no longer have a need to see. Similarly, macromutations that disrupt wing formation in an insect—ordinarily devastating in an environment where functional wings are essential equipment—might well be tolerated in an island setting where that species faces no need to fly. The processes that generate these exceptions, however, do not help to explain the origin of form such as occurs in the Cambrian explosion. Clearly, processes that result in a loss of form and structure cannot be credibly invoked to explain the origin of form and structure in the first place.
20. Darwin, On the Origin of Species, 108.
21. Løvtrup, “Semantics, Logic and Vulgate Neo-Darwinism,” 162.
22. Britten and Davidson, “Gene Regulation for Higher Cells,” 57.
23. Britten and Davidson, “Gene Regulation for Higher Cells,” 57. One exception to this rule are cells called “erythrocytes” in humans.
24. Britten and Davidson, “Gene Regulation for Higher Cells,” 57.
25. Britten and Davidson, “Gene Regulation for Higher Cells,” 353.
26. Cameron et al., “A Sea Urchin Genome Project,” 9514.
27. Oliveri, Tu, and Davidson, “Global Regulatory Logic for Specification of an Embryonic Cell Lineage.”
28. Davidson, The Regulatory Genome, 16.
29. Davidson, The Regulatory Genome, 16.
30. Davidson, “Evolutionary Bioscience as Regulatory Systems Biology,” 38.
31. Davidson, “Evolutionary Bioscience as Regulatory Systems Biology,” 40, emphasis added.
32. As Davidson explains, “Interference with expression of any [multiply linked dGRNs] by mutation or experimental manipulation has severe effects on the phase of development that they initiate. This accentuates the selective conservation of the whole subcircuit, on pain of developmental catastrophe” (Davidson and Erwin, “An Integrated View of Precambrian Eumetazoan Evolution,” 8).
33. Davidson, The Regulatory Genome, 195.
34. Davidson, “Evolutionary Bioscience as Regulatory Systems Biology,” 35–36.
Chapter 14: The Epigenetic Revolution
1. Spemann and Mangold, “Induction of Embryonic Primordia by Implantation of Organizers from a Different Species.”
2. Harvey, “Parthenogenetic Merogony or Cleavage Without Nuclei in Arbacia punctulata”; “A Comparison of the Development of Nucleate and Non-nucleate Eggs of Arbacia punctulata.”
3. Brachet, Denis, and De Vitry, “The Effects of Actinomycin D and Puromycin on Morphogenesis in Amphibian Eggs and Acetabularia mediterranea.”
4. Masui, Forer, and Zimmerman, “Induction of Cleavage in Nucleated and Enucleated Frog Eggs by Injection of Isolated Sea-Urchin Mitotic Apparatus.”
5. Müller and Newman, “Origination of Organismal Form,” 8.
6. Müller and Newman, “Origination of Organismal Form,” 8.
7. Müller and Newman, “Origination of Organismal Form,” 7.
8. Müller and Newman, “Origination of Organismal Form,” 7. Or as Müller also explains, the question of how “individualized constructional elements” are organized during “the evolution of organismal form” is “not satisfactorily answered by current evolutionary theories”; Müller, “Homology,” 57–58.
9. Levinton, Genetics, Paleontology, and Macroevolution, 485.
10. In 1942 Conrad Waddington coined the word “epigenetics” to refer to the study of “the processes involved in the mechanism by which the genes of the genotype bring about phenotypic eff
ects” (“The Epigenotype,” 1). Some more recent biologists have used it to refer to information in chromosomal structures that do not depend on the underlying DNA sequence. I will use it to refer to any biological information that is not encoded in a DNA sequence.
11. Goodwin, “What Are the Causes of Morphogenesis?”; Nijhout, “Metaphors and the Role of Genes in Development”; Sapp, Beyond the Gene; Müller and Newman, “Origination of Organismal Form”; Brenner, “The Genetics of Behaviour”; Harold, The Way of the Cell.
12. Harold, The Way of the Cell, 125.
13. Harold, “From Morphogenes to Morphogenesis,” 2774; Moss, What Genes Can’t Do. Of course, many proteins bind chemically with each other to form complexes and structures within cells. Nevertheless, these “self-organizational” properties do not fully account for higher levels of organization in cells, organs, or body plans. Or, as Moss has explained “Neither DNA nor any other aperiodic crystal constitutes a unique repository of heritable stability in the cell; in addition, the chemistry of the solid state does not constitute either a unique or even an ontologically or causally privileged basis for explaining the existence and continuity of order in the living world …” Moss, What Genes Can’t Do, 76.
14. Wells, “Making Sense of Biology,” 121.
15. Harold, The Way of the Cell, 125.
16. Ally et al., “Opposite-Polarity Motors Activate One Another to Trigger Cargo Transport in Live Cells”; Gagnon and Mowry, “Molecular Motors.”
17. Marshall and Rosenbaum, “Are There Nucleic Acids in the Centrosome?”
18. Poyton, “Memory and Membranes”; Edidin, “Patches, Posts and Fences.”
19. Frohnhöfer and Nüsslein-Volhard, “Organization of Anterior Pattern in the Drosophila Embryo by the Maternal Gene Bicoid”; Lehmann and Nüsslein-Volhard, “The Maternal Gene Nanos Has a Central Role in Posterior Pattern Formation of the Drosophila Embryo.”
20. Roth and Lynch, “Symmetry Breaking During Drosophila Oogenesis.”
21. Skou, “The Identification of the Sodium-Pump as the Membrane-Bound Na+ /K+-ATPase.”
22. Levin, “Bioelectromagnetics in Morphogenesis.”
23. Shi and Borgens, “Three-Dimensional Gradients of Voltage During Development.”
24. Schnaar, “The Membrane Is the Message,” 34–40.
25. Schnaar, “The Membrane Is the Message,” 34–40; Gabius et al., “Chemical Biology of the Sugar Code,” 740-764; Gabius, “Biological Information Transfer Beyond the Genetic Code: The Sugar Code,” 108–121.
26. Gabius et al., “Chemical Biology of the Sugar Code,” 741. See also Gabius, “Biological Information Transfer Beyond the Genetic Code: The Sugar Code,” 108–21.
27. Gabius, “Biological Information Transfer Beyond the Genetic Code,” 109; Gabius et al., “Chemical Biology of the Sugar Code,” 741.
28. Spiro, “Protein Glycosylation.”
29. Palade, “Membrane Biogenesis.”
30. Babu, Kriwacki, and Pappu, “Versatility from Protein Disorder”; Uversky and Dunker, “Understanding Protein Non-Folding”; Fuxreiter and Tompa, “Fuzzy Complexes.”
31. Wells, “Making Sense of Biology: The Evidence for Development by Design,” 121.
32. McNiven and Porter, “The Centrosome.”
33. Lange et al., “Centriole Duplication and Maturation in Animal Cells”; Marshall and Rosenbaum, “Are There Nucleic Acids in the Centrosome?”
34. Sonneborn, “Determination, Development, and Inheritance of the Structure of the Cell Cortex,” 1–13; Frankel, “Propagation of cortical differences in tetrahymena,” 607–623; Nanney, “The ciliates and the cytoplasm,” 163–170.
35. Moss, What Genes Can’t Do.
36. Harold, “From Morphogenes to Morphogenesis,” 2767.
37. See Müller and Newman, “The Origination of Organismal Form,” 7.
38. Thomson, “Macroevolution,” 107.
39. Miklos, “Emergence of Organizational Complexities During Metazoan Evolution.”
40. Gilbert, Opitz, and Raff, “Resynthesizing Evolutionary and Developmental Biology,” 361. The Brian Goodwin quotation is from How the Leopard Changed Its Spots.
41. Gilbert, Opitz, and Raff, “Resynthesizing Evolutionary and Developmental Biology.” Specifically, they argue that changes in morphogenetic fields might produce large-scale changes in the developmental programs and, ultimately, in the body plans of organisms. However, they offer no evidence that such fields—if indeed they exist—can be altered to produce advantageous variations in body plan, though such a condition is necessary to any successful causal theory of macroevolution.
42. Webster, How the Leopard Changed Its Spots, 33; Webster and Goodwin, Form and Transformation, x; Gunter Theißen, “The Proper Place of Hopeful Monsters in Evolutionary Biology,” 351; Marc Kirschner and John Gerhart, The Plausibility of Life, 13; Schwartz, Sudden Origins, 3, 299–300; Erwin, “Macroevolution Is More Than Repeated Rounds of Microevolution”; Davidson, “Evolutionary Bioscience as Regulatory Systems Biology,” 35; Koonin, “The Origin at 150,” 473–5; Conway Morris, “Walcott, the Burgess Shale, and Rumours of a Post-Darwinian World,” R928–R930; Carroll, “Towards a New Evolutionary Synthesis,” 27; Wagner, “What Is the Promise of Developmental Evolution?”; Wagner and Stadler, “Quasi-independence, Homology and the Unity-of Type”; Becker and Lönnig, “Transposons: Eukaryotic,” 529–39; Lönnig and Saedler, “Chromosomal Rearrangements and Transposable Elements,” 402; Müller and Newman, “Origination of Organismal Form,” 7; Kauffman, At Home in the Universe, 8; Valentine and Erwin, “Interpreting Great Developmental Experiments,” 96; Sermonti, Why Is a Fly Not a Horse?; Lynch, The Origins of Genome Architecture, 369; Shapiro, Evolution, 89, 128.
The perspective of Eugene Koonin, a biologist at the National Center for Biotechnology Information at the National Institutes of Health, provides just one good example of this skepticism. He argues: “The edifice of the modern synthesis has crumbled, apparently, beyond repair … The summary of the state of affairs on the 150th anniversary of the Origin is somewhat shocking. In the postgenomic era, all major tenets of the modern synthesis have been, if not outright overturned, replaced by a new and incomparably more complex vision of the key aspects of evolution. So, not to mince words, the modern synthesis is gone. What comes next? The answer suggested by the Darwinian discourse of 2009 is a postmodern state, not so far a postmodern synthesis. Above all, such a state is characterized by the pluralism of processes and patterns in evolution that defies any straightforward generalization.” Koonin, “The Origin at 150,” 473–75. David J. Depew and Bruce H. Weber, writing in the journal Biological Theory, are even more frank: “Darwinism in its current scientific incarnation has pretty much reached the end of its rope” (89–102).
Chapter 15: The Post-Darwinian World and Self-Organization
1. Conway Morris, “Walcott, the Burgess Shale and Rumours of a Post-Darwinian World,” R928.
2. Conway Morris, “Walcott, the Burgess Shale and Rumours of a Post-Darwinian World,” R930.
3. Mazur, The Altenberg 16: An Exposé of the Evolution Industry. See also Whitfield, “Biological Theory.”
4. Budd, quoted in Whitfield, “Biological Theory,” 282.
5. Valentine and Erwin, “Interpreting Great Developmental Experiments,” 97.
6. Endler, Natural Selection in the Wild, 46, 248; Lewontin, “Adaptation,” 212–30.
7. Gerhart and Kirschner, The Plausibility of Life: Resolving Darwin’s Dilemma, 10.
8. Kauffman, The Origins of Order: Self-Organization and Selection in Evolution.
9. In The Origins of Order, Kauffman seeks to show that self-organizational processes could help account for both the origin of the first life and the origin of subsequent forms of life, including new animal body plans. In Signature in the Cell, I examined Kauffman’s specific proposal for explaining the origin of the first life. Here I’ll examine his proposal for explaining the origin of animal form.
10. Kauffman,
The Origins of Order, 443.
11. Kauffman, The Origins of Order, 443.
12. Kauffman, The Origins of Order, 443.
13. Kauffman, The Origins of Order, 537.
14. Kauffman, The Origins of Order, 539.
15. Kauffman, The Origins of Order, 549–66.
16. Kauffman, The Origins of Order, 590.
17. Kauffman, The Origins of Order, 298.
18. Kauffman, The Origins of Order, 537, emphasis added.
19. Kauffman, At Home in the Universe, 68.
20. Kauffman, At Home in the Universe, 47–92.
21. Kauffman, At Home in the Universe, 71.
22. Kauffman, At Home in the Universe, 75–92.
23. Kauffman, At Home in the Universe, 86–88.
24. Kauffman, At Home in the Universe, 85, emphasis added.
25. Kauffman, At Home in the Universe, 53, 89, 102.
26. Kauffman, At Home in the Universe, 200.
27. Indeed, Kauffmann explicitly notes, “Mutants affecting early stages of development disrupt development more than do mutants affecting late stages of development. A mutation disrupting formation of the spinal column and cord is more likely to be lethal than one affecting the number of fingers that form” (At Home in the Universe, 200).
28. Newman, “Dynamical Patterning Modules.”
29. Newman, “Dynamical Patterning Modules,” 296; see also “The Developmental Genetic Toolkit and the Molecular Homology-Analogy Paradox.”
30. Newman, “Dynamical Patterning Modules,” 284.
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