Matthew Levy and Stanley L. Miller, “The stability of the RNA bases: Implications for the origin of life,” Proceedings of the National Academy of Sciences USA 95 (1998): pp.7933–7938.
Imagine trying to bake a loaf of bread--only the ingredients keep spoiling, or simply disappearing, before you can get them all together long enough for the bread to rise (not to mention make it into the oven). A highly analogous situation exists with the chemical precursors to the biomolecule RNA, thought by many to be the first self-replicating entity. “For a compound to be used in the first living organism,” observe Levy and Miller (Biochemistry, UC-San Diego), “it needs to be sufficiently stable so that the balance between synthesis and degradation does not result in vanishingly small concentrations.” The precursors to RNA, however--the nucleobases adenine (A), uracil (U), guanine (G), and cytosine (C)--don’t hang around for long at the temperatures postulated in the popular “hot origin-of-life” scenarios, where life arose, perhaps near deep-sea thermal vents, at temperatures between 80 and 100 degrees centigrade. Levy and Miller heated samples of A, U, G, C, and then determined their rates of decomposition. They found that “the rapid rates of hydrolysis [destruction by water] of the nucleobases A, U, G, C and T [thymine] at temperatures much above 0 degrees C would present a major problem in the accumulation of these presumed essential compounds on the early Earth” (p. 7933). Levy and Miller suggest that research should be directed instead at the possibility of a low-temperature origin of life, especially in light of other “stability” problems, including “the stability of ribose, the decomposition of nucleosides, and the hydrolysis of the phosphodiester bonds of RNA. Similar stability considerations would apply to any alternative pre-RNA backbone, e.g., peptide nucleic acids” (p. 7937).
Kathleen K. Smith and Richard A. Schneider, “Have gene knockouts caused evolutionary reversals in the mammalian first arch?” BioEssays 20 (1998): pp. 245-255.
Lisa Nagy, “Changing Patterns of Gene Regulation in the Evolution of Arthropod Morphology,” American Zoologist 38 (1998): 818-828.
It is possible to “knock out” (i.e., eliminate the activity of) genes in mice. This powerful experimental method enables developmental geneticists to study the function of the missing genes, by examining the defects their absence might cause. In several such experiments, in which perturbed genes played a role in the development of the first arch, where the bones of the jaw and inner ear arise, biologists claimed to have uncovered “reversions” to more primitive forms: that is, the phenotype caused by knocking out a mouse gene was thought to have revealed structures possessed by the evolutionary ancestors of mice. Smith and Schneider (Zoology, Duke University) examined these experiments critically, and argue that, on the contrary, “in none of the cases reported do the null mutant [knock-out] phenotypes show identity with, or close resemblance, to the character state found in mammalian ancestors or transitional forms” (p. 250). Rather, “each null mutation produces not only a differently shaped ectopic element, but also a dissimilar suite of associated disruptions, virtually none of which resembles any aspect of the primitive condition,” instead revealing structures which are “obviously pathological and unlike the primitive condition” (p. 252). Smith and Schneider express doubt that knock-out mutations will reveal much, or anything, about the course of evolution: “We conclude therefore that these experiments provide little information about the evolutionary transformations of the first arch” (p. 252). Nagy (Molecular Biology, University of Arizona) draws a similar moral from mutagenesis in flies: “The take home message is that mutagenesis in model systems does not undo evolution or reveal, in any direct fashion, the basis of evolutionary change” (p. 820).
Thomas C. Oden, “Without Excuse: Classic Christian Exegesis of General Revelation,” Journal of the Evangelical Theological Society 41 (1998): pp. 55–68.
Near the center of the debate about intelligent design within the science-and-theology community lies the question of the validity of general revelation--namely, the idea that one can have knowledge of God’s existence and character by observing natural things. Theological skeptics of intelligent design argue that even if design theory were possible scientifically (which most doubt), it would be a serious blunder to attempt to revive the bankrupt notion of general revelation. Natural theology finds no basis in a proper understanding of the Bible. The distinguished theologian and editor Thomas C. Oden (Drew University) dissents from this widely-held view. The earliest Christian theologians, he argues, all held strongly to the reality of general revelation. “There is a well-defined, reliable, pre-European, classical Christian teaching of general revelation,” Oden writes, “consensually received for a millennium before the Reformation that has been generally received and valued not only by the Lutheran and Reformed traditions but also by the evangelical and revivalist traditions” (p. 55). Focusing on the classic text of Romans 1:19–20, Oden examines the commentaries of what he calls “the universally-esteemed great doctors of the Church” (p. 56), such as Athanasius, John Chrysostom, Augustine, and Gregory of Nyssa. Oden concludes that “there is a substantive consensus of classic Christian commentary on Rom. 1:18ff that confirms with Paul that all humanity is offered some true, even if limited, knowledge of God by contemplating the majesty and goodness of God in the whole of creation” (p. 68).
Michael Ruse, “Darwinism and atheism: different sides of the same coin?” Endeavour 22 (1998): pp. 17–20.
The philosopher of science and historian Michael Ruse of the University of Guelph has long been one of the liveliest commentators on the relationship of science and religion in biology. Lately Ruse has been analyzing the role of “extrascientific” considerations (e.g., the notion of progress) in the origin and rise of evolutionary theory (see his book Monad to Man: The Concept of Progress in Evolutionary Biology, Harvard University Press, 1996). One such issue at the meeting-place of science, philosophy, and theology concerns whether the acceptance of Darwinian evolution entails atheism. In both his lectures and publications, Ruse has been at pains to stress that it does not. “Perhaps it is reasonable to be a Darwinian,” he writes, in the article cited above. “Perhaps it is reasonable to be an atheist. I am not at all convinced that the one implies the other” (p. 20). In developing this thesis, Ruse is trying to clear a middle ground between those who argue (on both the atheistic left and theological right) that evolution correctly grasped leaves any Creator worthy of the name largely unemployed and thus superfluous to our understanding of reality. Ruse offers counter-examples to this view, most notably Sir Ronald Fisher, the neo-Darwinian statistician, founder of population genetics, and practicing Anglican. But most of Ruse’s other examples seem to challenge his own view. While it is true that Darwinism does not strictly entail atheism, in the logical sense of a necessary consequence, there can be no doubt that most prominent evolutionary theorists, beginning with Darwin’s own grandfather Erasmus, opposed anything resembling Christian revelation, and can be described as only weakly deist (at best). In some cases, e.g., Theodosius Dobzhansky, the “God” they extolled was indistinguishable from pantheism. Moreover, Ruse says nothing about the dozens of cases, such as his friends E.O. Wilson and Richard Dawkins, or the British theorist John Maynard Smith, where the Christian theism of the scientist’s youth vanished like dew in bright sunshine following that scientist’s personal discovery of Darwinism. Ruse gently mocks what he calls the “hostility” to Darwinism of the 19th-century Princeton theologist Charles Hodge, who “thundered” that Darwinism “is atheism” (p. 17)--yet it seems clear that Hodge was a far better predictor of the difficulty of reconciling Darwinism and theism than Ruse allows.
Arcady R. Mushegian, James R. Garey, Jason Martin, and Leo X. Liu, “Large-Scale Taxonomic Profiling of Eukaryotic Model Organisms: A Comparison of Orthologous Proteins Encoded by the Human, Fly, Nematode, and Yeast Genomes,” Genome Research 5 (1998): pp. 590–598.
Ann-Sofie Rasmussen and Ulfur Arnason, “Phylogenetic Studies of Complete Mitochondrial DNA Molecules Place Cartilaginous Fishes Within the Tree of Bony Fishes,” Journal of Molecular Evolution 48 (1999): pp. 118–123.
“Increasing knowledge results in increasing pain,” said the writer of Ecclesiastes (1:18). Time was, an evolutionary systematist could point to cytochrome C (or some other protein), and say that the distibution of this molecule fully confirmed standard, morphologically-based relationships. But biological knowledge increases, and pain--well, let’s just say it’s a much trickier business these days to derive unequivocal phylogenies from molecules. In this study, Arcady Mushegian and his colleagues compared 36 proteins drawn from humans, arthropods (flies), nematodes (the worm C. elegans), and yeast. They discovered that “different proteins can generate different apparent phylogenetic tree topologies [see Figure 1], strongly suggesting that historical phylogenies should not be inferred based on a single protein-coding gene” (p. 596). As Figure 1 demonstrates, the genes used to construct Tree B (where flies and worms share a more recent common ancestor than either does with humans) give a different history than those in Tree A (where humans and flies share a more recent common ancestor than either does with worms). Rasmussen and Arnason (Genetics, University of Lund) provide another instance where asking genes for history may upset the “right” evolutionary tree.
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Figure 1. The three possible branching patterns for an evolutionary tree relating humans, arthropods, and nematodes (with yeast as the outgroup). 24 genes support Tree A, 11 genes support Tree B, and one gene supports Tree C. (Figure after Mushegian et al., 1998, p. 593.) |
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