31. Newman, “Dynamical Patterning Modules,” 284.
32. Newman, “Dynamical Patterning Modules,” 285.
33. Newman, “Dynamical Patterning Modules,” 285.
34. Newman, “Animal Egg as Evolutionary Innovation,” 570.
35. Newman, “Animal Egg as Evolutionary Innovation”; “Dynamical Patterning Modules.”
36. Newman, “Animal Egg as Evolutionary Innovation,” 470–71; see also Newman and Bhat, “Dynamical Patterning Modules: Physico-Genetic Determinants.”
37. In a 2011 paper, Newman attempts to account for the origin of the crucial egg stage in animal development, a long-unsolved puzzle for neo-Darwinism. He does this by proposing, again, an interplay between the developmental-genetic regulatory toolkit and a host of self-organizational and epigenetic processes. He envisions the egg stage arising in three steps. First, he sees the interaction between “the metazoan developmental-genetic toolkit and certain physical processes” organizing “primitive animal body plans independently of an egg stage.” Second, he envisions the emergence of a “proto-egg” arising as the result of the “adaptive specialization of cells” as they are released from aggregates of other cells. Third, he notes that since self-organizing processes (such as “egg-patterning processes”) are known to reorganize the contents of the cellular cytoplasm during development, these same processes could have done so in the past, further sculpting the proto-egg into something more like the egg stage in animal development observed today. He insists, moreover, that the structures induced by these egg-patterning processes are not adaptive “in the sense of having been gradually arrived at through multiple cycles of selection,” but instead that they have resulted from self-organizational physical and chemical processes. See Newman, “Animal Egg as Evolutionary Innovation: A Solution to the ‘Embryonic Hourglass’ Puzzle,” 467–83.
38. Khalturin et al., “More Than Just Orphans: Are Taxonomically-Restricted Genes Important in Evolution?” 404–413; Tautz and Domazet-Lošo, “The evolutionary origin of orphan genes,” 692–70; Beiko, “Telling the Whole Story in a 10,000-Genome World,” 34.
39. See the discussion in Chapter 14, pages 277–81.
40. See the discussion in Chapter 14, pages 277–81.
41. Pivar, Lifecode; On the Origin of Form; Prigogine, Nicolis, and Babloyantz, “Thermodynamics of Evolution”; Wolfram, “A New Kind of Science,” 398.
42. Meyer, Signature in the Cell, 254–55.
43. Yockey, “A Calculation of the Probability of Spontaneous Biogenesis by Information Theory,” 380.
44. For example, see the popular computer game among amateur programmers, the “Game of Life,” created by the British mathematician John Horton Conway.
45. Kauffman, “The End of a Physics Worldview: Heraclitus and the Watershed of Life.”
46. Kauffman, “The End of a Physics Worldview: Heraclitus and the Watershed of Life.”
Chapter 16: Other Post-Neo-Darwinian Models
1. See Gould, “Is a New and General Theory of Evolution Emerging?” 120.
2. Gould does not use the term “macromutation” anywhere in his famous 1980 article (“Is a New and General Theory of Evolution Emerging?”). He does, however, use the term “micromutation” (see 120) and challenges the sufficiency of accumulated micromutations to explain “macroevolution” (a term used throughout the article).
3. Goldschmidt, The Material Basis of Evolution, 395.
4. The rejection of large-scale mutations affecting morphology and function as adaptive nonstarters emerged early and persisted as one of the defining aspects of the neo-Darwinian synthesis. Neo-Darwinian paleontologist and macroevolution theorist Jeffrey Levinton, for instance, gives expression to the widely held skepticism about the evolutionary plausibility of such mutants in his major textbook dealing with macroevolution:
As a general rule, major developmental mutants give a picture of hopeless monsters, rather than hopeful change. Epigenetic and genetic pleiotropy [i.e., side effects] both impart great burden to any major developmental perturbation. Thus it is unlikely that mutants affecting any fundamental prepattern in development are likely to produce a functional organism. Genes that activate switches in prepatterns are not sufficiently isolated in effect on other parts of the phenotype to expect major saltations. The cyclops mutant of the [brine shrimp] Artermia is lethal. The homeotic mutants of Drosophila melanogaster suffer similar fates… . Disruptions, i.e., mutants, have drastic effects on other parts of the phenotype… . Thus, the accumulated evidence suggests that major developmental mutants are of minor significance in evolution. The side effects are drastic. (Genetics, Paleontology, and Macroevolution, 252–54)
5. The central difficulty with relying on developmental macromutations to generate innovations in form, many neo-Darwinians noted, arises from the consequence of rapidly changing a system of genetic and developmental switches directed toward producing one “target” (stable adult form) to another system of such switches directed toward producing another form. Geneticist Bruce Wallace, trained by Theodosius Dobzhansky at Columbia University, explains: “The Bauplan [body plan] of an organism … can be thought of as the arrangement of genetic switches that control the course of the embryonic and subsequent development of the individual; such control must operate properly both in time generally and sequentially in the separately differentiated tissues. Selection, both natural and artificial, that leads to morphological change and other developmental modification does so by altering the settings and triggerings of these switches… . The extreme difficulty encountered when attempting to transform one organism into another but still functioning one lies in the difficulty in resetting a number of the many controlling switches in a manner that still allows for the individual’s orderly (somatic) development” (“Adaptation, Neo-Darwinian Tautology, and Population Fitness,” 70). Our discussion in Chapter 13 suggests that the need to alter these functionally integrated switches also presents an obstacle to the efficacy of the neo-Darwinian mechanism.
6. Gould, “Is a New and General Theory of Evolution Emerging?” 127.
7. Of course, the range of post-neo-Darwinian theories is not exhausted by this chapter’s survey of four prominent contenders. In a recent review paper, evolutionary biologist Armin Moczek, of Indiana University, examined three additional ideas attempting to move beyond what Moczek calls the “unrealistic and unproductive” assumptions of gene-centered neo-Darwinian theory. Those ideas are, respectively: (1) the theory of “facilitated variation” (Gerhart and Kirschner, “The Theory of Facilitated Variation”), the theory of “genetic accommodation” and “niche construction theory.” See Moczek, “The Nature of Nurture and the Future of Evodevo.” Short explanations and critiques of these models are posted on the website for this book, www.darwinsdoubt.com.
8. Gould, “Is a New and General Theory of Evolution Emerging?”
9. Gilbert, Opitz, and Raff, “Resynthesizing Evolutionary and Developmental Biology,” 362.
10. The assumption that evolutionary biologists could ignore the role of developmental biology derived in part from the need for population geneticists to make simplifying assumptions in order “to keep the mathematics tractable,” note developmental biologists Michael Palopoli and Nipam Patel. As they explain, “It was assumed that evolutionary changes in genotype are translated into phenotypic changes by an undefined set of epigenetic laws; in other words, developmental evolution was ignored [by neo-Darwinism] in order to focus on the dynamics of allele frequency changes in populations” (“Neo-Darwinian Developmental Evolution, 502).
11. Raff, The Shape of Life.
12. Schwartz, “Homeobox Genes, Fossils, and the Origin of Species”; Schwartz, Sudden Origins; Goodwin, How the Leopard Changed Its Spots; Carroll, Endless Forms Most Beautiful.
13. Experimental mutagenesis of fruit flies (Drosophila melanogaster) began in earnest at Columbia University, in the breeding laboratories of Thomas H. Morgan and others, during the first decade of the twentieth
century.
14. Meyer et al., Explore Evolution, 108.
15. Body Plans, http://ncse.com/book/export/html/2585 (accessed November 6, 2012).
16. Normal Protein, http://ncse.com/book/export/html/2580 (accessed November 6, 2012).
17. Body Plans, http://ncse.com/book/export/html/2585 (accessed November 6, 2012).
18. Prud’homme, Gompel, and Carroll, “Emerging Principles of Regulatory Evolution.”
19. Prud’homme, Gompel, and Carroll, “Emerging Principles of Regulatory Evolution,” 8605.
20. Hoekstra and Coyne note explicitly that the best examples of alleged CRE-induced mutations showed “losses of traits rather than the origin of new traits” (“The Locus of Evolution,” 1006).
21. Hoekstra and Coyne, “The Locus of Evolution,” 996.
22. Schwartz, Sudden Origins, 3.
23. Schwartz, Sudden Origins, 13. According to Schwartz, “At the genetic level, major morphological novelty can indeed be accomplished in the twinkling of an eye. All that is necessary is that homeobox genes are either turned on or they are not” (362).
24. McGinnis and Kurziora, “The Molecular Architects of Body Design,” 58.
25. Lindsey and Grell, Guide to Genetic Variations of Drosophila melanogaster.
26. Lewis, “A Gene Complex Controlling Segmentation in Drosophila”; Peifer and Bender, “The Anterobithorax and Bithorax Mutations of the Bithorax Complex”; Fernandes et al., “Muscle Development in the Four-Winged Drosophila and the Role of the Ultrabithorax Gene.”
27. Szathmáry, “When the Means Do Not Justify the End,” 745.
28. Scott and Carroll, “The Segmentation and Homeotic Gene Network in Early Drosophila Development.”
29. Davidson and Erwin, “An Integrated View of Precambrian Eumetazoan Evolution.”
30. Schwartz, Sudden Origins, 362.
31. Szathmáry, “When the Means Do Not Justify the End,” 745.
32. Schwartz, Sudden Origins, 362.
33. Szathmáry, “When the Means Do Not Justify the End,” 745.
34. Panganiban et al., “The Origin and Evolution of Animal Appendages.”
35. Instead, epigenetic information and structures actually determine the function of many Hox genes. This can be seen dramatically when the same Hox gene (as determined by nucleotide sequence homology) regulates the development of the strikingly different (i.e., classically nonhomologous) anatomical features found in different phyla. For instance, in arthropods, the Hox gene Distal-less is required for the normal development of limbs, but homologous genes are found in vertebrates (e.g., the Dlx gene in mice), where the gene also plays a key role in limb development—albeit a vertebrate (internal skeleton), not arthropod (external skeleton) limb. Distal-less homologues in yet other phyla, such as echinoderms, regulate the development of tube feet and spines—again, anatomical features classically not homologous to arthropod or vertebrates limbs.
In each case, the roles of the Hox genes are governed “top-down” by the higher-level organismal contexts in which they occur. Panganiban et al., “The Origin and Evolution of Animal Appendages.”
36. Despite all this, some evolutionary theorists have argued that the emergence of Hox genes in Precambrian organisms may have triggered the Cambrian explosion by providing the raw materials for the diversification of body plans (Carroll, Patterns and Processes of Vertebrate Evolution). Yet, in addition to those difficulties already noted, recent studies have highlighted another problem with attributing the origin of body plans to Hox genes. Hox genes first emerged long before the diversification of the various bilaterian phyla, suggesting—because of the length of the time lag—that something else must have responsible for the Cambrian explosion. As a paper in the journal Science explains, “The temporal lag between the initial construction of these networks and the eventual appearance of bilaterian fossils suggests that the solution to the dilemma of the Cambrian explosion lies not solely with this genomic and developmental potential, but instead must also be found in the ecology of the Cambrian radiation itself” (Erwin et al., “The Cambrian Conundrum,” 1095). See also de Rosa et al., “Hox Genes in Brachiopods and Priapulids and Protostome Evolution.”
37. Lynch, “The Origins of Eukaryotic Gene Structure,” 454.
38. Lynch, “The Origins of Eukaryotic Gene Structure,” 450. He actually goes even further, contending that “random genetic drift can impose a strong barrier to the advancement of molecular refinements by adaptive processes.” Lynch, “Evolutionary Layering and the Limits to Cellular Perfection.”
39. Jurica, “Detailed Closeups and the Big Picture of Spliceosomes,” 315. See also Butcher, “The Spliceosome as Ribozyme Hypothesis Takes a Second Step,” 12211–12; Nilsen, “The Spliceosome: The Most Complex Macromolecular Machine in the Cell?” 1147–49.
40. Quoted in Azar, “Profile of Michael Lynch,” 16015.
41. On my website for this book, www.darwinsdoubt.com, I explain why the origin of the eukaryotic cell presents such a formidable challenge to all theories of unguided evolution.
42. Lynch, “The Origins of Eukaryotic Gene Structure,” 450–68 (emphasis added).
43. See Lynch, “The Frailty of Adaptive Hypotheses for the Origin of Organismal Complexity,” 8597–604.
44. Gauger points out that Lynch, “offers no explanation of how nonadaptive forces can produce the functional genomic and organismal complexity we observe in modern species.” [Ann Gauger, “The Frailty of the Darwinian Hypothesis, Part 2.”] Jerry Coyne observes much the same: “Both drift and natural selection produce genetic change that we recognize as evolution. But there’s an important difference. Drift is a random process, while selection is the anti-thesis of randomness… . As a purely random process, genetic drift can’t cause the evolution of adaptations. It could never build a wing or an eye. That takes nonrandom natural selection.” [Coyne, Why Evolution Is True, 123.]
45. Lynch and Abegg, “The Rate of Establishment of Complex Adaptations,” 1404.
46. Lynch and Abegg, “The Rate of Establishment of Complex Adaptations,” 1414.
47. Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” 3.
48. Axe, “The Limits of Complex Adaptation: An Analysis Based on a Simple Model of Structured Bacterial Populations,” 3.
49. Darwin, On the Origin of Species, 134–38. Darwin’s own theory of transmission genetics, dubbed “pangenesis,” postulated that a host of minute heredity particles, which he called “gemmules,” accumulated in the reproductive organs of organisms, carrying information about the life history and environmental circumstances of the parent. This information would then be transmitted at reproduction to offspring, allowing the “inheritance” of “acquired” characteristics.
50. Darwin. The Illustrated Origin of Species (6th edition), 95, writes, “I think there can be no doubt that use in our domestic animals has strengthened and enlarged certain parts, and disuse diminished them; and such modifications are inherited.”
51. Some question exists about the historical accuracy of calling these twenty-first-century ideas “neo-Lamarckian” in light of the actual content of Jean-Baptiste de Lamarck’s views when compared with the enormous growth of knowledge about heredity over the past two hundred years. Given that Jablonka adapts the term “Lamarckism” to her own position, however, I follow that practice, with the caveats about differences in content noted.
52. Jablonka and Raz, “Transgenerational Epigenetic Inheritance,” 168.
53. Jablonka and Raz, “Transgenerational Epigenetic Inheritance,” 138, emphasis added.
54. Jablonka and Raz, “Transgenerational Epigenetic Inheritance,”162.
55. Shapiro, Evolution, 2.
56. Shapiro contends that the neo-Darwinian insistence on fundamental randomness arose for philosophical, not empirical (or observational) reasons, having to do with the exclusion of “supernatural intervention” in the origin of organisms.
; 57. Shapiro, Evolution, 12.
58. Shapiro, Evolution, 14.
59. Shapiro, Evolution, 14.
60. Shapiro, Evolution, 16.
61. Shapiro, Evolution, 16.
62. Shapiro, Evolution, 14.
63. As biologist Bénédicte Michel observes, “Clearly, it is important for bacteria to keep all levels of the SOS response under tight control. There is no utility to the organism of using error-prone polymerases longer than absolutely necessary” (“After 30 Years, the Bacterial SOS Response Still Surprises Us,” 1175).
64. Shapiro, “Darwin’s Black Box: The Biochemical Challenge to Evolution-Book Reviews.”
Chapter 17: The Possibility of Intelligent Design
1. As Dawkins explains: “Natural selection, the blind, unconscious, automatic process which Darwin discovered and which we now know is the explanation for the existence and apparently purposeful form of all life, has no purpose in mind. It has no mind and no mind’s eye” (The Blind Watchmaker, 5).
2. Mayr, Foreword, in Ruse, ed., Darwinism Defended, xi–xii.
3. Ayala, “Darwin’s Greatest Discovery,” 8572.
4. As Dawkins notes: “Biology is the study of complicated things that give the appearance of having been designed for a purpose” (The Blind Watchmaker, 1). Crick likewise explains: “Organisms appear as if they had been designed to perform in an astonishingly efficient way, and the human mind therefore finds it hard to accept that there need be no Designer to achieve this” (What Mad Pursuit, 30). Lewontin also observes that living organisms “appear to have been carefully and artfully designed” (“Adaptation”).
5. Dawkins, River Out of Eden, 17.
6. Dawkins, The Blind Watchmaker, 1.
7. Gillespie, Charles Darwin and the Problem of Creation, 83–108.
8. Thaxton, Bradley, and Olsen, The Mystery of Life’s Origin, 211.
9. We have observational evidence in the present that intelligent investigators can (and do) build contrivances to channel energy down nonrandom chemical pathways to bring about some complex chemical synthesis, even gene building. May not the principle of uniformity then be used in a broader frame of consideration to suggest that DNA had an intelligent cause at the beginning? (Thaxton, Bradley, and Olsen, The Mystery of Life’s Origin, 211).
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