Science in Christian Perspective

 

 

Stepping Back to Look at Neo-Darwinism

David F. Siemens, Jr.*
2703 E. Kenwood St.
Mesa, AZ 85213-2384

From: PSCF 48 (June 1996): 104-107.

There is a serious problem with the way evangelical scientists view evolution. For example, the "Call for Papers: 1994 Annual Meeting Symposium" asks "whether the scientific data justify extrapolating from microevolutionary changes produced by natural selection to the production of new body plans and structures."1 The answer must be "No," for the question prejudges the problem.2 The first difficulty is that natural selection does not produce microevolutionary changes. It does not, indeed cannot, drive mutations. It merely sorts among such mutations as they occur.3

The introductory question of the call is broader: "Is the neo-Darwinian mechanism of selection of random mutations adequate for the creation of major biological innovations?" The answer is still "No." The accumulation of mutations, translocations, transpositions, and inversions seems to produce "good" species within genera or families. The Hawaiian Drosophila come immediately to mind. Ecological niches occupied and behavioral changes in timing and mating signals prevent interbreeding in the wild.4 Genetic modifications affect, and even control, all these. But no accumulation of mutations in the small genome of an entity like a dipteran can produce the large genome of a vertebrate. Also, any radical change in an essential gene will almost certainly reduce viability. It may well be lethal.

A First Look: Color

If we step back from a simple consideration of mutations, we may ask whether there is any way in which a vital gene can take on new functions without sacrificing the old.5 The answer appears to be "Yes." A crude example occurs in color vision. Human beings, like many other mammals, have genes for color vision on different chromosomes. The visual pigment giving blue sensitivity is produced by a gene on an autosome. The two visual pigments giving green and red sensitivity are produced by genes on X, the sex chromosome.6 This is why color-blindness is thought of as a sex-linked recessive. Both genes on X are very similar. The visual pigments for which they code are just different enough to shift their peak spectral absorption somewhat. This shifting produces very subtle differences in color vision.7 The pigment giving blue sensitivity is also similar, as is rhodopsin, which gives the rods monochromatic sensitivity. Fish produce rhodopsin. Blue vision is widespread among mammals. American monkeys have a gene for red visual pigment on the sex chromosome. Chimpanzees add green visual pigment. The simplest biological explanation for these phenomena is that the original rhodopsin gene was duplicated and the replication mutated. This produced the continued ability to see plus the new ability to differentiate some colors in bright light. Later, a similar process produced the added ability to detect red, giving enhanced color discrimination. Finally, the new ability to see green produced full trichromatic vision.8 At each stage, enhanced sensitivity would plausibly be selected for, whereas modification of the original genes without duplication would surely be deleterious, except perhaps for creatures like blind cave fish. There is another piece of evidence that bolsters this explanation: some human X-chromosomes carry more than one copy of the gene for green visual pigment.9 Those with this unusual genotype have a normal phenotype.

One may also ask whether an organism can acquire new genes from outside the species. The answer appears to be "Yes." Germs are known to transfer resistance to antibiotics from one bacterial species to another. Some viruses transfer genetic material between plants. More recently, evidence has been found that transfer by arthropods can occur among insects. So viruses, bacteria and small arthropods are potential vectors.10

The Genetic Attic

Recent evidence shows that a duplicated gene may become quiescent rather than taking on new duties. Researchers found a gene that they estimate has not been active for about five million years in the mouse genome.11 This gives additional support to the view that the large mammalian genome results from the accumulation of duplicate DNA. Some of this may be currently without function, "junk DNA." However, I keep reading of functions, especially control functions, discovered for some introns which had been written off as "junk."12 The most surprising development to me is that a functional coding sequence may be embedded in an intron.13 This brings to mind the long list of vestigial organs once given,14 at least mainly the product of ignorance of the endocrine system. So it behooves us to say only that parts of the genome are currently without known function, rather than declaring them without function. Unfortunately, where careful scientists insert qualifications, popular and semi-popular reports often omit them.

Managing Structure: Homologies

Scientists long ago observed that embryos develop in an orderly fashion. More recently they have discovered that aspects of the progression are controlled by strings of genes called homeoboxes. The nature and distribution of these control sequences also bear on the possibility that reduplication and modification of genes may produce radically different body plans and structures. A relatively small number of homeobox genes were found to lie sequentially on a Drosophila chromosome. During embryogenesis, they were activated sequentially to control the development of segments on the cephalo-caudal axis. Mutations of these genes produce leg-like structures in place of antennae, four wings in place of the normal two wings and halteres, or embryonic death.

Using probes derived from Drosophila genes, geneticists have discovered a much larger number of mammalian homeobox genes. They function like the dipteran genes, although the radically different body plans necessarily produce clearly different effects. A fruit fly, larva or adult, has clearly delimited segments whose sequential development can be tied directly to specific homeoboxes. A mammalian embryo has a much more complex pattern of development, requiring more than one sequence. Nevertheless, it appears that strings of such genes are activated sequentially to control the various stages of development. Further, the Drosophila sequence and the several mammalian sequences are clearly similar.15

A different type of control gene contains a sequence of thymine and adenine residues (abbreviated as T and A), whose duplication produces the name, TATA-boxes. These genes are even more broadly conserved.16 Apoptosis is controlled by similar genes in Drosophila and Xenopus.17 The list may be extended by those familiar with the literature, for 40% of the genes are homologous in Drosophila and Homo.18

Obviously, the total embryonic environment has much to do with the effect of any gene. There is no way that the gene controlling production of legs, wings, and halteres on the three segments that fuse to form the insect thorax can trigger similar organs in a chordate, let alone a mammal. Further, as scientists gain more understanding of the work of control genes, they find them acting in more complex ways, being reactivated a second time during development, or even apparently having a function in the adult organism.19 Despite all these complexities of function, it has been shown that a mammalian gene can replace a defective dipteran gene, and even a yeast gene. Apparently, the structure of some vital genes has been conserved while duplicated genes have mutated, combined, or otherwise changed to take on different functions.

Bumps Under The Carpet

Besides gene duplication and mutation, there are additional possibilities for change. Polyploidy, hybridization, chromosome breakage and recombination, reassortment of introns and exons within and among genes, including transpositions and inversions, along with position effects, may combine to effect more radical changes than most of us expect. I have not encountered any indication that we have deciphered the factors that differentiate the relatively simple segmentation of annelids from the more complex patterns of arthropods, or the gene-activation pattern transforming the bilateral embryonic body into a radially organized starfish or sea urchin. Until all such matters have been deciphered and it can be shown that no genetic process can connect one pattern of development to another, we must not claim that evolutionary descent is impossible. To suggest that evolution is not reasonable because simple mutation cannot produce the required changes, is to bear false witness.

Where Next

Do these considerations show that an updated neo-Darwinian mechanism has provided an adequate explanation for the development of radial, externally supported and internally supported animals from a single aboriginal form? No. Do they suggest experiments to transform "primitive" animals into "advanced" forms? No, for all are, ex hypothesi, the latest result of eons of modification and selection.20 But they definitely narrow the gap between some diverse structures. Also, they suggest the kind of information which may narrow the gap even more. They clearly need to be faced by honest investigators.21

1996

 Notes

1ASA/CSCA Newsletter, (March/April 1994): 3.

2I have assumed that the scientist is fully open to evidence that macroevolution may have occurred and is unwilling to bias the investigation. However, the question is purely rhetorical to some, for they are certain that macroevolution has not, or cannot, occur. Both 144-hour Creationists and those who believe that the geologic eras saw multiple creations that suffered only microevolutionary change fall here. The adherent to dogmatic evolutionism is oppositely biased. I thank the anonymous referee for calling my attention to this matter.

3This view may require modification. See David S. Thaler, "The Evolution of Genetic Intelligence," Science 264 (8 April 1994): 224f. The original report, John Cairns, Julie Overbaugh and Stephan Miller, "The Origin of Mutants," Nature 335 (8 September 1988): 142-145, produced numerous responses. See ibid. 336 (3 November 1988): 21f; (8 December): 525-528; 337 (12 January 1989): 119, 123f. Both Cairns' response (336: 528, notes 7-10) and Thaler, op. cit., add other studies.

Samuel L. Scheiner, in his review of Stephen C. Stearns, The Evolution of Life Histories, notes the broad range of matters which require consideration in the evaluation of scientific theories of descent. See Science 258 (11 December 1992): 1820-1822.

4Kenneth Y. Kaneshiro, "Speciation in the Hawaiian Drosophila," BioScience 38 (April 1988): 258-263 says that the number of species is both 509 and about 640-730 on p. 258. Roger Lewin, "Hawaiian Drosophila: Young Islands, Old Flies," Science 229 (13 September 1985): 1072-1074 says over 800 on p. 1072. Fred Hapgood, "Fruit Fly Fandango," Science 84 (September 1984): 68-74, notes behavioral isolation.

We may be seeing speciation in the split of a fruit fly, Rhagoletis pomonella, into populations adapted to apple and hawthorn, with their different schedules. See Scientific American (February 1989): 22, 24. The original reports are Jeffrey L. Feder, Charles A. Chilcote and Guy L. Bush, "Genetic Differentiation Between Sympatric Host Races of the Apple Maggot Fly Rhagoletis pomonella," Nature 336 (3 November 1988): 61-64; Bruce A. McPherson, D. Courdney Smith and Stewart H. Berlocher, "Genetic Differences Between host races of Rhagoletis pomonella, ibid. 64-66; D. Courtney Smith, "Heritable Divergence of Rhagoletis pomonella Host Races by Seasonal Asynchrony," ibid. 66f. This last adds dogwood to the hosts.

5See Russell F. Doolittle and Peer Bork, "Evolutionarily Mobile Modules in Proteins," Scientific American (October 1993): 50-56; Jrgen Brosius, "Retrosponsons<|><|>Seeds of Evolution," Science 251 (15 February 1991): 753; Stephen C. Stearns, ibid. 259 (5 March 1993): 1476.

6Both these genes map to Xq28. See "Genome Maps III," bound in Science 258 (2 October 1992): center; Douglas Vollrath, Jeremy Nathans and Ronald W. Davis, "Tandem Array of Human Visual Pigment Genes at Xq28," ibid. 240 (17 June 1988): 1669-1672.

  The gene for blue sensitivity maps to chromosome 7. See Jeremy Nathans, "The Genes for Color Vision," Scientific American (February 1989): 42-49; Geoffrey Montgomery, "Color Perception: Seeing with the Brain," Discover (December 1988): 52-59, sidebar on 58.

7See Deborah Franklin, "Newswatch," Science 86 (July/August): 6; Vollrath, Nathans and Davis, op. cit.; Shannath L. Merbs and Jeremy Nathans, "Absorption Spectra of the Hybrid Pigments Responsible for Anomalous Color Vision," Science 258 (16 October 1992): 464-466.

8See Maureen Neitz, Jay Neitz and Gerald H. Jacobs, "Spectral Tuning of Pigments Underlying Red-Green Color Vision," Science 252 (17 May 1991): 971-974. South American monkeys have a single X-linked pigment apiece which is, in the species examined, from 96% to 98% identical to the human red pigment.

9See Franklin, op. cit.

10Margaret A. Houck et al., "Possible Horizontal Transfer of Drosophila Genes by the Mite Proctolaelaps regalis," Science 253 (6 September 1991): 1125-1129.

11See "Reviving Old Mouse DNA," Science 264 (1 April 1994): 27. The original report is in Proceedings of the National Academy of Sciences for 15 February.

12See, for example, Marcia Barinaga, "Introns Pop up in New Places What Does It Mean?" Science 250 (14 December 1990): 1512; John Abelson, "Recognition of tRNA Precursors: A Role for the Intron," ibid. 255 (13 March 1992): 1390; M. Irene Baldi et al., "Participation of the Intron in the Reaction Catalyzed by the Xenopus tRNA Splicing Endonuclease," ibid. 1404-1408; Marlene Belfort, "An Expanding Universe of Introns," ibid. 262 (12 November 1993): 1009f.

13See Roger Lewin, "Reverse Transcriptase in Introns," Science 229 (13 September 1985): 1073.

14Robert Weiderscheim, Der Bau das Menschen (1895; 3rd ed., 1902), is commonly cited. I was unable to confirm the given number, about 180, in its translation, The Structure of Man (1895).

15See, for example, Jean L. Marx, "Homeobox Linked to Gene Control, Science 242 (18 November 1988): 1008f; John F. Fallon et al., ibid. 264 (1 April 1994): 105-107; John Rennie, "Old Gene, New Trick: The Not-so-holy Engrailed Reveals the Path of Evolution," Scientific American (December 1989): 30f; Eddy M. De Robertis, Guillermo Oliver and Christopher V. E. Wright, "Homeobox Genes and the Vertebrate Body Plan," ibid. (July 1990): 46-52.

16See Michael Gregory Peterson et al., "Functional Domains and Upstream Activation Properties of Cloned Human TATA Binding Protein," Science 248 (29 June 1990): 1625-30; C. Cheng Kao et al.,"Cloning of a Transcriptionally Active Human TATA Binding Factor," ibid 1646-50.

17See Clark Coffman, William Harris and Chris Kintner, "Xotch, the Xenopus Homolog of Drosophila Notch," Science 249 (21 September 1990): 1438-1441.

18See Ross H. Crozier, Science 245 (21 July 1989): 314.

19See John Benditt, "POU! Goes the Homeobox: Developmental DNA Sequences Are Found in Puzzling Places," Scientific American (February 1989): 20, 22.

20Population genetics adds further complexity by warning us that selection is not simple. Specialists in various fields will surely add to the list of relevant considerations.

21Stephen C. Meyer (Symposium, ASA Annual Meeting, August 9, 1993) implicitly made a point that all should remember: evolutionary descent does not preclude design. Alternatively phrased, a mechanism does not have to be mechanistic, naturalistic, and materialistic.