Darwinism's failure as a predictive model XIV

 Darwinism's predictions 

Cornelius G Hunter 

A fundamental concept in evolutionary theory is the inheritance of genetic variations via blood lines. (Forbes) This so-called vertical transmission of heritable material means that genes, and genomes in general, should fall into a common descent pattern, consistent with the evolutionary tree. Indeed, such genes are often cited as a confirmation of evolution. But as more genomic data have become available, an ever increasing number of genes have been discovered that do not fit the common descent pattern because they are missing from so many intermediate species. (Andersson and Roger 2002; Andersson and Roger 2003; Andersson 2005; Andersson, Sarchfield and Roger 2005; Andersson 2006; Andersson et. al. 2006; Andersson 2009; Andersson 2011; Haegeman, Jones and Danchin; Katz; Keeling and Palmer; Richards et. al 2006a; Richards et. al 2006b; Takishita et. al.; Wolf et. al.)

 

This type of pattern is also found for genome architecture features which are sporadically distributed and then strikingly similar in distant species. In fact these similarities do not merely occur twice, in two distant species. They often occur repeatedly in a variety of otherwise distant species. This is so widespread that evolutionists have named the phenomenon “recurrent evolution.” As one paper explains, the recent explosion of genome data reveals “strikingly similar genomic features in different lineages.” Furthermore, there are “traits whose distribution is ‘scattered’ across the evolutionary tree, indicating repeated independent evolution of similar genomic features in different lineages.” (Maeso, Roy and Irimia) 

One example is the uncanny similarity between the kangaroo and human genomes. As one evolutionist explained: “There are a few differences, we have a few more of this, a few less of that, but they are the same genes and a lot of them are in the same order. We thought they’d be completely scrambled, but they’re not.” (Taylor)

 

It is now well recognized that this prediction has failed: “Vertical transmission of heritable material, a cornerstone of the Darwinian theory of evolution, is inadequate to describe the evolution of eukaryotes, particularly microbial eukaryotes.” (Katz) And these sporadic, patchy patterns require complicated and ad hoc scenarios to explain their origin. As one paper explained, the evolution of a particular set of genes “reveals a complex history of horizontal gene transfer events.” (Wolf et. al.) The result is that any pattern can be explained by arranging the right mechanisms. Features that are shared between similar species can be interpreted as “the result of a common evolutionary history,” and features that are not can be interpreted as “the result of common evolutionary forces.” (Maeso, Roy and Irimia)

 

These common evolutionary forces are complex and must have been created by evolution. They can include horizontal (or lateral) gene transfer, gene loss, gene fusion, and even unknown forces. For instance, one study concluded that the best explanation for the pattern of a particular gene was that it “has been laterally transferred among phylogenetically diverged eukaryotes through an unknown mechanism.” (Takishita et. al.) Even with the great variety of mechanisms available, there still remains the unknown mechanism.

References 

Andersson, J., A. Roger. 2002. “Evolutionary analyses of the small subunit of glutamate synthase: gene order conservation, gene fusions, and prokaryote-to-eukaryote lateral gene transfers.” Eukaryotic Cell 1:304-310.

 

Andersson, J., A. Roger. 2003. “Evolution of glutamate dehydrogenase genes: evidence for lateral gene transfer within and between prokaryotes and eukaryotes.” BMC Evolutionary Biology 3:14.

 

Andersson, J. 2005. “Lateral gene transfer in eukaryotes.” Cellular and Molecular Life Sciences 62:1182-97.

 

Andersson, J., S. Sarchfield, A Roger. 2005. “Gene transfers from nanoarchaeota to an ancestor of diplomonads and parabasalids.” Molecular Biology and Evolution 22:85-90.

 

Andersson, J. 2006. “Convergent evolution: gene sharing by eukaryotic plant pathogens.” Current Biology 16:R804-R806.

 

Andersson, J., R. Hirt, P. Foster, A. Roger. 2006. “Evolution of four gene families with patchy phylogenetic distributions: influx of genes into protist genomes.” BMC Evolutionary Biology 6:27.

 

Andersson, J. 2009. “Horizontal gene transfer between microbial eukaryotes.” Methods in Molecular Biology 532:473-487.

 

Andersson, J. 2011. “Evolution of patchily distributed proteins shared between eukaryotes and prokaryotes: Dictyostelium as a case study.” J Molecular Microbiology and Biotechnology 20:83-95.

 

Haegeman, A., J. Jones, E. Danchin. 2011. “Horizontal gene transfer in nematodes: a catalyst for plant parasitism?.” Molecular Plant-Microbe Interactions 24:879-87.

Katz, L. 2002. “Lateral gene transfers and the evolution of eukaryotes: theories and data.” International J. Systematic and Evolutionary Microbiology 52:1893-1900.

 

Keeling, P., J. Palmer. 2008. “Horizontal gene transfer in eukaryotic evolution,” Nature Reviews Genetics 9:605-18.

 

Maeso, I, S. Roy, M. Irimia. 2012. “Widespread Recurrent Evolution of Genomic Features.” Genome Biology and Evolution 4:486-500.

 

Richards, T., J. Dacks, J. Jenkinson, C. Thornton, N. Talbot. 2006. “Evolution of filamentous plant pathogens: gene exchange across eukaryotic kingdoms.” Current Biology 16:1857-1864.

 

Richards, T., J. Dacks, S. Campbell, J. Blanchard, P. Foster, R. McLeod, C. Roberts. 2006. “Evolutionary origins of the eukaryotic shikimate pathway: gene fusions, horizontal gene transfer, and endosymbiotic replacements.” Eukaryotic Cell 5:1517-31.

 

Takishita, K., Y. Chikaraishi, M. Leger, E. Kim, A. Yabuki, N. Ohkouchi, A. Roger. 2012. “Lateral transfer of tetrahymanol-synthesizing genes has allowed multiple diverse eukaryote lineages to independently adapt to environments without oxygen.” Biology Direct 7:5.

 

Taylor, R. 2008. “Kangaroo genes close to humans,” Reuters, Canberra, Nov 18.

Wolf, Y., L. Aravind, N. Grishin, E. Koonin. 1999. “Evolution of aminoacyl-tRNA synthetases--analysis of unique domain architectures and phylogenetic trees reveals a complex history of horizontal gene transfer events.” Genome Research 9:689-710. 

 

Darwinism's failure as a predictive model XI

 Darwinism's predictions 

Cornelius G Hunter 

Early in the twentieth century scientists studied blood immunity and how immune reaction could be used to compare species. The blood studies tended to produce results that parallel the more obvious indicators such as body plan. For example, humans were found to be more closely related to apes than to fish or rabbits. These findings were said to be strong confirmations of evolution. In 1923 H. H. Lane cited this evidence as supporting “the fact of evolution.” (Lane, 47) Later in the century these findings continued to be cited in support of evolution. (Berra, 19; Dodson and Dodson, 65)

 

But even by mid century contradictions to evolutionary expectations were becoming obvious in serological tests. As J.B.S.Haldane explained in 1949, “Now every species of mammal and bird so far investigated has shown quite a surprising biochemical diversity by serological tests. The antigens concerned seem to be proteins to which polysaccharides are attached.” (quoted in Gagneux and Varki)

 

Indeed these polysaccharides, or glycans, did not fulfill evolutionary expectations. As one paper explained, glycans show “remarkably discontinuous distribution across evolutionary lineages,” for they “occur in a discontinuous and puzzling distribution across evolutionary lineages.” (Bishop and Gagneux) These glycans can be (i) specific to a particular lineage, (i) similar in very distant lineages, (iii) and conspicuously absent from very restricted taxa only.

Here is how another paper described glycan findings: “There is also no clear explanation for the extreme complexity and diversity of glycans that can be found on a given glycoconjugate or cell type. Based on the limited information available about the scope and distribution of this diversity among taxonomic groups, it is difficult to see clear trends or patterns consistent with different evolutionary lineages.” (Gagneux and Varki) 

References 

Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.

 

Bishop J., P. Gagneux. 2007. “Evolution of carbohydrate antigens--microbial forces shaping host glycomes?.” Glycobiology 17:23R-34R.

 

Dodson, Edward, Peter Dodson. 1976. Evolution: Process and Product. New York: D. Van Nostrand Company.

 

Gagneux, P., A. Varki. 1999. “Evolutionary considerations in relating oligosaccharide diversity to biological function.” Glycobiology 9:747-755.

Lane, H. 1923. Evolution and Christian Faith. Princeton: Princeton University Press.

Darwinism's failure as a predictive model VIII

 Darwin's Predictions 

Cornelius G Hunter 

The pentadactyl structure—five digits (four fingers and a thumb for humans) at the end of the limb structure—is one of the most celebrated proof texts for evolution. The pentadactyl structure is found throughout the tetrapods and its uses include flying, grasping, climbing and crawling. Such diverse activities, evolutionists reason, should require diverse limbs. There seems to be no reason why all should need a five digit limb. Why not three digits for some, eight for others, 13 for some others, and so forth? And yet they all are endowed with five digits. As Darwin explained, “What can be more curious than that the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise, and the wing of the bat, should all be constructed on the same pattern, and should include similar bones, in the same relative positions?” (Darwin, 382)

 

Such a suboptimal design must be an artefact of common descent—a suboptimal design that was handed down from a common ancestor rather than specifically designed for each species. And the common descent pattern formed by this structure is often claimed as strong evidence for evolution. (Berra, 21; Campbell et. al., 509; Futuyma, 47; Johnson and Losos, 298; Johnson and Raven, 286; Mayr, 26) One text calls it a “classic example” of evolutionary evidence. (Ridley, 45) 

Such a suboptimal design must be an artefact of common descent—a suboptimal design that was handed down from a common ancestor rather than specifically designed for each species. And the common descent pattern formed by this structure is often claimed as strong evidence for evolution. (Berra, 21; Campbell et. al., 509; Futuyma, 47; Johnson and Losos, 298; Johnson and Raven, 286; Mayr, 26) One text calls it a “classic example” of evolutionary evidence. (Ridley, 45)

 

But this prediction is now known to be false as the digit structure in the tetrapods does not conform to the common descent pattern. In fact, appendages have various digit structures and they are distributed across the species in various ways. This is found both in extant species and in the fossil record. As evolutionist Stephen Jay Gould explained, “The conclusion seems inescapable, and an old ‘certainty’ must be starkly reversed.” (Gould)

 

This means that evolutionists cannot model the observed structures and pattern of distribution merely as a consequence of common descent. Instead, a complicated evolutionary history is required (Brown) where the pentadactyl structure re-evolves in different lineages, and appendages evolve, are lost, and then evolve again. And as one recent study concluded, “Our phylogenetic results support independent instances of complete limb loss as well as multiple instances of digit and external ear opening loss and re-acquisition. Even more striking, we find strong statistical support for the re-acquisition of a pentadactyl body form from a digit-reduced ancestor. … The results of our study join a nascent body of literature showing strong statistical support for character loss, followed by evolutionary re-acquisition of complex structures associated with a generalized pentadactyl body form.” (Siler and Brown) 

References 

Berra, Tim. 1990. Evolution and the Myth of Creationism. Stanford: Stanford University Press.

Brown, R., et. al. 2012. “Species delimitation and digit number in a North African skink.” Ecology and Evolution 2:2962-73.

Campbell, Neil, et. al. 2011. Biology. 5th ed. San Francisco: Pearson.

 

Darwin, Charles. 1872. The Origin of Species. 6th ed. London: John Murray.

http://darwin-online.org.uk/content/frameset?itemID=F391&viewtype=text&pageseq=1

 

Futuyma, Douglas. 1982. Science on Trial: The Case for Evolution. New York: Pantheon Books.

 

Gould, Steven Jay. 1991. “Eight (or Fewer) Little Piggies.” Natural History 100:22-29.

 

Johnson, G., J. Losos. 2008. The Living World. 5th ed. New York: McGraw-Hill.

 

Johnson, G., P. Raven. 2004. Biology. New York: Holt, Rinehart and Winston.

 

Mayr, Ernst. 2001. What Evolution Is. New York: Basic Books.

 

Ridley, Mark. 1993. Evolution. Boston: Blackwell Scientific.

Siler C., R. Brown. 2011. “Evidence for repeated acquisition and loss of complex body-form characters in an insular clade of Southeast Asian semi-fossorial skinks.” Evolution 65:2641-2663.

Darwinism's failure as a predictive model VII

 Darwin's Predictions 

Cornelius G Hunter 

In the 1960s molecular biologists learned how to analyze protein molecules and determine the sequence of amino acids that comprise a protein. It was then discovered that a given protein molecule varies somewhat from species to species. For example, hemoglobin, a blood protein, has similar function, overall size and structure in different species. But its amino acid sequence varies from species to species. Emile Zuckerkandl and Linus Pauling reasoned that if such sequence differences were the result of evolutionary change occurring over the history of life, then they could be used to estimate past speciation events—a notion that became known as the molecular clock. (Zuckerkandl and Pauling)

In later decades this concept of a molecular clock, relying on the assumption of a roughly constant rate of molecular evolution, became fundamental in evolutionary biology. (Thomas, et. al.) As the National Academy of Sciences explained, the molecular clock “determines evolutionary relationships among organisms, and it indicates the time in the past when species started to diverge from one another.” (Science and Creationism, 3) Indeed the molecular clock has been extolled as strong evidence for evolution and, in fact, a common sentiment has been that evolution was required to explain these evidences. As a leading molecular evolutionist wrote, the molecular clock is “only comprehensible within an evolutionary framework.” (Jukes, 119, emphasis in original) The claim that the molecular clock can only be explained by evolution is, however, now a moot point as the mounting evidence shows that molecular differences often do not fit the expected pattern. The molecular clock which evolutionists had envisioned does not exist. The literature is full of instances where the molecular clock concept fails. For example, it was found early on that different types of proteins must evolve at very different rates if there is a molecular clock. For example the fibrinopeptide proteins in various species must have evolved more than five hundred times faster than the histone IV protein. Furthermore, it was found that the evolutionary rate of certain proteins must vary significantly over time, between different species, and between different lineages. (Thomas, et. al.; Andrews, 28)

The proteins relaxin, superoxide dismutase (SOD) and the glycerol-3-phosphate dehydrogenase (GPDH), for example, all contradict the molecular clock prediction. On the one hand, SOD unexpectedly shows much greater variation between similar types of fruit flies than it does between very different organisms such as animals and plants. On the other hand GPDH shows roughly the reverse trend for the same species. As one scientist concluded, GPDH and SOD taken together leave us “with no predictive power and no clock proper.” (Ayala)

Evolutionists are finding growing evidence that the purported rates of molecular evolution must vary considerably between species for a wide range of taxa, including mammals, arthropods, vascular plants, and even between closely related lineages. As one study concluded, “The false assumption of a molecular clock when reconstructing molecular phylogenies can result in incorrect topology and biased date estimation. … This study shows that there is significant rate variation in all phyla and most genes examined …” (Thomas, et. al.)

Evolutionists continue to use the molecular clock concept, but the many correction factors highlight the fact that the sequence data are being fit to the theory rather than the other way around. As one evolutionist warned, “It seems disconcerting that many exceptions exist to the orderly progression of species as determined by molecular homologies; so many in fact that I think the exception, the quirks, may carry the more important message.” (Schwabe) 

References 

ndrews, Peter. 1987. “Aspects of hominoid phylogeny” in Molecules and Morphology in Evolution, ed. Colin Patterson. Cambridge: Cambridge University Press.

Ayala, F. 1999. “Molecular clock mirages.” BioEssays 21:71-75.

Jukes, Thomas. 1983. “Molecular evidence for evolution” in: Scientists Confront Creationism, ed. Laurie Godfrey. New York: W. W. Norton.

Schwabe, C. 1986. “On the validity of molecular evolution.” Trends in Biochemical Sciences 11:280-282.

Science and Creationism: A View from the National Academy of Sciences. 2d ed. 1999. Washington, D.C.: National Academy Press.

Thomas, J. A., J. J. Welch, M. Woolfit, L. Bromham. 2006. “There is no universal molecular clock for invertebrates, but rate variation does not scale with body size.” Proceedings of the National Academy of Sciences 103:7366-7371.

Zuckerkandl, E., L. Pauling. 1965. “Molecules as documents of evolutionary history.” J Theoretical Biology 8:357-366.

 

On Darwinism's failure as a predictive model VI

 By Cornelius G Hunter 

Histones are proteins which serve as the hubs about which DNA is wrapped. They are highly similar across vastly different species which means they must have evolved early in evolutionary history. As one textbook explains, “The amino acid sequences of four histones are remarkably similar among distantly related species. … The similarity in sequence among histones from all eukaryotes indicates that they fold into very similar three-dimensional conformations, which were optimized for histone function early in evolution in a common ancestor of all modern eukaryotes.” (Lodish et. al., Section 9.5) And this high similarity among the histones also means they must not tolerate change very well, as another textbook explains: “Changes in amino acid sequence are evidently much more harmful for some proteins than for others. … virtually all amino acid changes are harmful in histone H4. We assume that individuals who carried such harmful mutations have been eliminated from the population by natural selection.” (Alberts et. al. 1994, 243)

So the evolutionary prediction is that in these histone proteins practically all changes are deleterious: “As might be expected from their fundamental role in DNA packaging, the histones are among the most highly conserved eucaryotic proteins. For example, the amino acid sequence of histone H4 from a pea and a cow differ at only at 2 of the 102 positions. This strong evolutionary conservation suggests that the functions of histones involve nearly all of their amino acids, so that a change in any position is deleterious to the cell.” (Alberts et. al. 2002, Chapter 4) 

This prediction has also been given in popular presentations of the theory: “Virtually all mutations impair histone’s function, so almost none get through the filter of natural selection. The 103 amino acids in this protein are identical for nearly all plants and animals.” (Molecular Clocks: Proteins That Evolve at Different Rates)

But this prediction has turned out to be false. An early study suggested that one of the histone proteins could well tolerate many changes. (Agarwal and Behe) And later studies confirmed and expanded this finding: “despite the extremely well conserved nature of histone residues throughout different organisms, only a few mutations on the individual residues (including nonmodifiable sites) bring about prominent phenotypic defects.” (Kim et. al.)

Similarly another paper documented these contradictory results: “It is remarkable how many residues in these highly conserved proteins can be mutated and retain basic nucleosomal function. … The high level of sequence conservation of histone proteins across phyla suggests a fitness advantage of these particular amino acid sequences during evolution. Yet comprehensive analysis indicates that many histone mutations have no recognized phenotype.” (Dai et. al.) In fact, even more surprising, many mutations actually raised the fitness level. (Dai et. al.) 

References 

Agarwal, S., M. Behe. 1996. “Non-conservative mutations are well tolerated in the globular region of yeast histone H4.” J Molecular Biology 255:401-411.

Alberts, Bruce., D. Bray, J. Lewis, M. Raff, K. Roberts, J. Watson. 1994. Molecular Biology of the Cell. 3d ed. New York: Garland Publishing.

Alberts, Bruce., A. Johnson, J. Lewis, et. al. 2002. Molecular Biology of the Cell. 4th ed. New York: Garland Publishing. http://www.ncbi.nlm.nih.gov/books/NBK26834/

Dai, J., E. Hyland, D. Yuan, H. Huang, J. Bader, J. Boeke. 2008. “Probing nucleosome function: a highly versatile library of synthetic histone H3 and H4 mutants.” Cell 134:1066-1078.

Kim, J., J. Hsu, M. Smith, C. Allis. 2012. “Mutagenesis of pairwise combinations of histone amino-terminal tails reveals functional redundancy in budding yeast.” Proceedings of the National Academy of Sciences 109:5779-5784.

Lodish H., A. Berk, S. Zipursky, et. al. 2000. Molecular Cell Biology. 4th ed. New York: W. H. Freeman. http://www.ncbi.nlm.nih.gov/books/NBK21500/

“Molecular Clocks: Proteins That Evolve at Different Rates.” 2001. WGBH Educational Foundation and Clear Blue Sky Productions.