Why Wrested Scriptures is wrong on evolution - Part 6

One of the main problems with Ron Abel’s attack on evolution in Wrested Scriptures was his complete failure to properly define evolution, or use his terms consistently. Instead of referring to evolution as fact (common descent) and evolution as theory (modern synthetic theory) he used terms such as ‘horizontal differentiation’ and ‘vertical evolution’ which are hardly standard, and result in a conflation of common descent with the theoretical mechanism proposed to explain it.

This is seen clearly in his attack on the genetic evidence for evolution. In his first two parts (palaeontology and morphology/embryology/comparative anatomy), his arguments were loosely attacking the evidence for common descent. In his third part, he changes approach and attacks the theoretical mechanism, rather than remaining consistent and looking at evidence for common descent as provided by genetics. Although Abel wrote his book well before the genomics revolution, if he had done his research properly, not only would he have recognised the difference between common descent and the modern synthetic theory of evolution, he would have recognised that as early as 1965, biologists had considered the possibility of using amino acid sequences to demonstrate common descent:

"It will be determined to what extent the phylogenetic tree, as derived from molecular data in complete independence from the results of organismal biology, coincides with the phylogenetic tree constructed on the basis of organismal biology. If the two phylogenetic trees are mostly in agreement with respect to the topology of branching, the best available single proof of the reality of macro-evolution would be furnished. Indeed, only the theory of evolution, combined with the realization that events at any supramolecular level are consistent with molecular events, could reasonably account for such a congruence between lines of evidence obtained independently, namely amino acid sequences of homologous polypeptide chains on the one hand, and the finds of organismal taxonomy and paleontology on the other hand. Besides offering an intellectual satisfaction to some, the advertising of such evidence would of course amount to beating a dead horse. Some beating of dead horses may be ethical, when here and there they display unexpected twitches that look like life." – Zuckerkandl, E., Pauling L (1965) "Evolutionary Divergence and Convergence in Proteins." in Evolving Genes and Proteins, p. 101.

This is the genetic evidence that Abel should have referred to if he was to keep his argument consistent. As I’ve stated repeatedly, comparative genomics alone makes the case for common descent irrefutable, with the presence of shared identical genetic errors (ERVs, retrotransposons, pseudogenes) at identical places in human and ape genomes confirming human-ape common ancestry. Arguments about plant breeding and Drosophila genetics not only show that he failed to understand the point, but also failed to understand evolutionary genetics.

Abel offered this advice to the Christadelphian trying to refute the genetic evidence for evolution:

1. Evidence required - Experimental evidence to prove that chance factors can elaborate the structural complexities of creatures.
2. Evidence lacking

• Although it is true that selective breeding has produced many varieties of plants and animals which may, under carefully controlled conditions, breed true to their new type, the fact that almost without exception, such new types would not be viable in nature is very strong presumption that evolution is unlikely to have been much helped by such processes.
• Indications of diversity on the same level of organization (e.g., Drosophila - the fruit fly) do not prove that present organization has proceeded from single-celled creatures to complex placentae.
• Years of labour, and millions of dollars of research have gone into unlocking the secrets of genetic codes. If anything, this would indicate deliberate planning and highly intelligent understanding behind its formation. It remains to be proven that it could occur by chance.

Abel’s failure to properly differentiate between fact and theory means that his attack on the genetic evidence for evolution is dead in the water. Irrespective of whether the modern evolutionary synthesis needs revision or replacement, the facts of common descent and large scale evolutionary change need to be explained either by the MES or any other theory of evolution. Problems – real or imagined – in the MES no more invalidate the fact of common descent than the inability of general relativity to explain gravity at the quantum level makes gravitational attraction suddenly go away.

Arguably the most powerful demonstration [1] of common descent is the presence of ERV inclusions in the same position in the genome of related species. John Coffin, an acknowledged expert in virology notes that:

Because the site of integration in the genome, which comprises some three billion base pairs in humans, is essentially random, the presence of an ancient provirus at exactly the same position in different, but related, species cannot occur by chance, but must be a consequence of integration into the DNA of a common ancestor of all the species that contain it. It evolution of retroviruses follows, therefore, that we can infer what viruses were present millions of years ago by examining the distribution of endogenous proviruses in modern species. [2]

In a frequently cited paper, Coffin and Johnson pointed [3] out how retroviral inclusions could be employed to reconstruct primate phylogenies or evolutionary family trees using the principle that retroviruses, once fixed in the genome of a species will be inherited by its descendants.

Coffin and Johnson used human endogenous retroviruses - most of the HERV families are found in apes and Old World monkeys. The HERVs used in their study are:

the result of integration events that took place between 5 and 50 million years ago, as indicated by the distribution of specific proviruses at the same integration sites (or loci) among related species. The evolution of primates has been the subject of intense study for well over a century, providing a well established phylogenetic consensus with which to compare and evaluate the performance of ERVs as phylogenetic markers.[4]

What Coffin and Johnson are pointing out towards the end is that we have a fairly reliable evolutionary family tree based on physical characteristics which they used to see how well family trees constructed using ERV data compared with the consensus tree.

Although the technical aspects of constructing such molecular trees are sophisticated, the basic principle behind it is fairly straightforward. An ERV proviral sequence that is selectively neutral will eventually accumulate mutations. If two species share a recent common ancestor, then the ERV inclusions they share will differ by only a small number of mutations, while species that share a remote ancestor will have their common ERV inclusion differing by significantly more mutations. Using sophisticated statistical tools, a family tree can be constructed from the molecular data.

ERV inclusions as Coffin and Johnson point out [5] have three sources of information that can be used to construct phylogenetic trees:

• The distribution of ERV inclusions among related species
• Accumulated mutations in proviral sequences, which allow an estimate of genetic distance
• Sequence divergence between the LTRs at each end of the ERV inclusion, which is a source of information unique to endogenous retroviruses.

With respect to the first point, both the huge size of the vertebrate genome and the random nature of retroviral integration, it is highly unlikely that one will find multiple ERV inclusions at the same location. As the authors point out:

Therefore, an ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place. Furthermore, integrated proviruses are extremely stable: there is no mechanism for removing proviruses precisely from the genome, without leaving behind a solo LTR or deleting chromosomal DNA. The distribution of an ERV among related species also reflects the age of the provirus: older loci are found among widely divergent species, whereas younger proviruses are limited to more closely related species. [6]

The second point is fairly straightforward, as it is similar to the principle underlying other sequence-based phylogenetic analytical methods. As proviral sequences are selectively neutral, they will tend to accumulate mutations at the rate of their occurrence. Two species that have only diverged recently will only differ by a small number of mutations at their common proviral sequence, while those that diverged in the remote past will differ by a larger number of mutations.

The final point - unique to ERVs - is the sequence divergence between the LTRs at either end of the proviral sequence. Of importance here is the fact that as a consequence of reverse transcription, both LTRs will be identical at the time of integration. Johnson and Coffin again:

Furthermore, both clusters are predicted to have similar branching patterns as determined by the phylogenetic history of the host species, with similar branch lengths. Thus, each tree displays two estimates of host phylogeny, both of which are derived from the evolution of an initially identical sequence. As we shall see, deviation of actual trees from this prediction provides a powerful means of testing the assumptions and detecting events other than neutral accumulation of mutations in the evolutionary history of a species.[7]

What did Johnson and Coffin find? Lets look at the distribution of the ERVs analysed. In their words:

Three of the loci, HERV-KC4, HERV-KHML6.17, and RTVL-Ia, were detectable in the genomes of OWMs and hominoids, but not New World monkeys, and therefore integrated into the germ line of a common ancestor of the Old World lineages. HERV-K18, RTVL-Ha, and RTVL-Hb were found exclusively in humans, gorillas, chimpanzees, and bonobos, and thus are consistent with a gorilla/chimpanzee/human clade. None of the loci was detected in New World monkeys. [8]

This data is perfectly explained by common descent. To reiterate an “ERV locus shared by two or more species is descended from a single integration event and is proof that the species share a common ancestor into whose germ line the original integration took place.” Johnson and Coffin found many loci shared by these primate species, some shared only by humans, chimps, bonobos and gorillas, some shared only by old world monkeys and hominoids (humans and great apes). This data is consistent with an evolutionary origin of these species, but impossible to explain by special creation without invoking a credulity-stretching concatenation of coincidence.

Estimates of integration time from data obtained from the 5’-LTR and 3’-LTR sequences were also consistent with predictions from common descent:

To estimate the age of each provirus the human/chimpanzee distances from each tree were used to calibrate the rate of molecular evolution at each locus…The most recent common ancestor of humans and chimpanzees lived approximately 4.5 million years ago…so dividing the distance between the human and chimpanzee sequences (substitutions per site) by this number gives rates ranging from 2.3 to 5.0 x 10-9 substitutions per site per year. These numbers are similar to the estimated rates of evolution for pseudogenes and noncoding regions of mammalian genes…Applying each rate to the divergence between the 5’ and 3’ LTRs of the same locus gives integration times consistent with estimates based on species distribution. [9]

Most of the ERVs analysed produced phylogenetic trees consistent with expectation. Their conclusions:

The HERVs analyzed above include six unlinked loci, representing five unrelated HERV sequence families. Except where noted, these sequences gave trees that were consistent with the well established phylogeny of the old world primates, including OWMs, apes, and humans… Phylogenetic analysis using HERV LTR sequences gives rise to trees with a predictable topology, on which is superimposed the phylogeny of the host taxa, and allows ready detection of conversion events.[10]

Evolutionary family trees constructed from ERV data, showing strong agreement with the existing family trees. (Source: Johnson, Coffin.)

In short - we share ERVs with primates at identical places in our genomes which are readily explained by common descent. Furthermore, this is a powerful tool which allows generation of evolutionary family trees. This is but part of the evidence for 'vertical evolution' from genetics, to use Abel's term consistently, and it is compelling evidence for common descent.

Genetic evidence for speciation.

Abel’s insistence on “[e]xperimental evidence to prove that chance factors can elaborate the structural complexities of creatures” repeats the old creationist canard that evolution is about chance. That is misleading [11]. While genetic mutations are random, natural selection is very much a deterministic process.

Selection acts on new genetic diversity, which is produced by a number of mechanisms:

• Point mutation: this is the most common form of mutation, and occurs when the nucleotide at a site in the genome is replaced by a different nucleotide. Some mutations are silent; others can result in a faulty gene product, while others can be beneficial.
• Insertion and deletion: these mutations occur when one or more nucleotides are inserted into, or deleted from a gene. Amino acids are encoded by three consecutive nucleotides, so if these insertions are not multiples of three, the result will be a frameshift mutation that will result in a truncated gene.
• Gene duplication: occasionally, genes (or even whole chromosomes) can be copied, resulting in more than one copy. Mutations in the extra copy can result in a decayed, non-functional gene (pseudogene) or it can result in a gene with a different function, which can allow new functionality to evolve.
• Whole Genome duplication: genomic analysis of many species shows that duplication of the whole genome has occurred in the remote past.
• Insertion of transposons: these are a class of mobile genetic elements that copy and paste, or cut and paste themselves from one part of the genome to another part. Retrotransposons copy themselves via an RNA intermediate, while DNA transposons achieve this transposition without the need for an RNA intermediate. Transposition can cause disease, but has also been linked to the evolution of new functionality.
• Integration of proviral sequences into host genomes: retroviruses, unlike DNA viruses encode their genetic material in RNA. They are able to insert a DNA copy of themselves into the host genome. If they insert themselves into the germline, they can be passed onto the next generation. Depending on where they insert themselves, they can alter the expression of nearby genes. Elements of the proviral sequence can be co-opted by the host genome for completely different uses.
• Horizontal gene transfer: the transfer of genetic elements from one species to another is quite common in bacteria, but has been noted in metazoans. The transferring of antibiotic resistance between different bacterial species is one notable example of horizontal gene transfer.

Some of these changes are deleterious, while some are beneficial. Many other are neutral and may convey an advantage to the population should environmental conditions change later. Contrary to the special creationist distortion of modern evolutionary biology, there are a number of ways in which beneficial mutations occur on which natural selection can work.

Furthermore, natural selection acting on genetic novelty is not the only mechanism of evolutionary change. The neutral theory of evolution argues that evolutionary change at the molecular level can occur through random drift of selectively neutral mutants.

Some mutations are harmful, some are beneficial but others are neutral. Collyer ignores the fact that a mutation that is beneficial in one environment may be positively harmful in another. The literature is replete with examples of beneficial mutations:

• A point mutation in the apolipoprotein A gene results in the creation of a mutant version of apolipoprotein A, apoA-_IM. This beneficial mutation has been linked with reduced rates of atherosclerosis in those heterozygous for the apoA-_IM mutation. [12] The clinical significance of this mutation has been explored in many studies. [13][14]
• The CCR5 gene codes for a chemokine receptor that, along with the CD4 T cell co-receptor is used by the HIV-1 virus as an entry point. A mutation in the CCR5 gene conveys resistance to HIV infection in people homozygous for the mutation, while HIV-1 infected individuals heterozygous for the mutation have a two to three year delay before they develop AIDS. The particular mutation is a 32 base pair deletion that results in loss of the CCR5 receptor. [15]
• Bacteria have evolved the ability to metabolise nylon breakdown products. This was achieved by a frameshift mutation which created a unique enzyme that gave the bacteria the opportunity to access a never-before utilised food source. [16]
• In 2008, the evolutionary biologist Richard Lenski published a landmark paper on the evolution by a colony of E. coli bacteria of the ability to metabolise citrate under oxic conditions, something that E. coli is not normally able to do. Over the previous twenty years, Lenski had cultured 12 colonies of E. coli, taking samples every 500 generations to provide a “fossil record”. After 31,500 generations, one colony evolved the ability to metabolise citrate in an oxic environment. The two hypotheses to explain this were (1) an extremely rare mutation or (2) a mutation that was contingent on an earlier mutation to evolve the ability to metabolise citrate. Lenski’s analysis favoured the latter, “Our results instead support the hypothesis of historical contingency, in which a genetic background arose that had an increased potential to evolve the Cit_ phenotype.” [17]
• Evolution of vertebral steroid receptors and the endocrine systems associated with them involved duplication of an ancestral steroid receptor gene, and mutation of the duplicate. [18][19]
• Evidence of chromosomal translocation and segmental duplication in Cryptococcus neoformans. [20]
• Genome duplication in yeast as a source of evolutionary novelty. [21]
• Whole genome duplication as a source of genetic variety is not restricted to yeasts. Examination of the genomes of chordates has shown the existence of multiple copies of genes in the same gene family. None of this is remotely controversial; as long ago as 1999, one paper noted:

Duplication of genes and entire genomes are two of the major mechanisms that facilitated the increasing complexity of organisms in the evolution of life. Gene duplications might be responsible for the functional diversification of genes, the creation of gene families and the generally increased genomic, and possibly also phenotypic, complexity. Protostomes, such as Drosophila, and deuterostome ancestors of vertebrates tend to have single copies of genes whereas chordate genomes typically have more genes, often four; the copies belong to the same gene family. [22]

• Proviral elements from ancient retroviral infections have served as the source of genetic novelty. Placental morphogenesis would not be possible without the cooption of an ancient retroviral envelope protein to perform an entirely different task. [23]
• Horizontal gene transfer in bacteria is responsible for more than just the transfer of antibiotic resistance. One example involves the Salmonella PhoP-PhoQ system which senses environmental magnesium ions, allowing the bacterium to tell whether it is inside a host cell. If this is the case, it activates a molecular pathway that permits it to survive inside the cell. The genes that permit Salmonella to do this are not part of its original genome but were obtained by horizontal gene transfer. [24]
• Evolution of complexity has been simulated and occurs in a Darwinian manner. [25]

The creationist claim that mutations are harmful to life and often lethal is simply wrong, and ignores the fact that as we have shown, mutations can be beneficial. More importantly, he overlooks the fact that most mutations are neutral. Lenski’s long term evolutionary experiment highlights the fact that neutral mutations can linger in the genome until another mutation arrives which effects a beneficial phenotypic change. The average human being has around 175 mutations, [26] according to one study so clearly, most of these are not life-threatening, and otherwise we wouldn’t be here! Really serious mutations tend to be purged from the gene pools via purifying selection. Crippling mutations such as those causing Huntingdon’s disease, CADASIL or other genetic disorders are noticeable because of their characteristic phenotype. Neutral mutations are invisible from a phenotypic perspective, so the special creationist simply overlooks their existence.

Likewise, the creationist attacks on the Drosophila experiments demonstrate specific ignorance of what these experiments are aimed to achieve. [27] The authors of a recent review paper on experimental evolution using a Drosophila model point out:

Experimental evolution with laboratory populations is an alternative tool with which to study adaptation. One of the most attractive applications of experimental evolution is to create a replicated set of populations that have been differentiated relative to replicated control populations, using a well-defined selection protocol, and then compare the allele frequencies at various loci for associations between particular types of phenotypic and genetic differentiation. In short, laboratory evolution allows biologists to use strong inference tests of hypotheses concerning phenotypic and genetic responses to selection. In addition, the recent development of cost-effective genomic tools has allowed broad and systematic assays of the molecular foundations of the effects of experimental evolution. [28]

If one remembers that evolution is a change in allele frequencies in a population, then the 'problem' posed by creationists becomes simply an artefact of the straw man they have created. Examples of evolution observed in Drosophila abound:

Stress-resistance characters respond to direct and reverse selection. Laboratory selection for increased resistance to starvation and desiccation produces rapid responses within populations of D. melanogaster, and high heritability estimates have been reported for both traits. Direct selection for increased starvation (Rose system “SO” and SB” lines) and desiccation (Rose system “D” lines) resistance results in a correlated increase in longevity in the absence of acute starvation or desiccation, along with decreased fecundity...Furthermore, some experiments suggest that lines selected for increased desiccation resistance have decreased preadult viability and slower development time than control lines. There appear to be complex trade-offs connecting resource acquisition during larval stages, adult stress resistance, and life history generally. [29]

Pseudocomparative surveys and reverse-selection experiments reveal correlations between stress resistance and life history characters. The mean longevity of Drosophila populations has been demonstrated to change as a result of manipulating the age of reproduction in a population over multiple generations. Furthermore, longer-lived lines (Rose system “O” lines) have generally been found to tolerate starvation and desiccation significantly better than lines with shorter average lifespans (Rose system “B” lines). These pseudocomparative results were interpreted to mean that resistance to starvation and desiccation might be general physiological mechanisms necessary for maintaining health at late ages. [30]

It hardly needs stressing that there is no ‘limit’ to evolutionary change, but a reference to documented speciation [31] in Drosophila should make this clear, and prevent any further creationist attempts to peddle the usual misunderstandings about Drosophila experiments.

The final – and most important – point focuses on the fact that modern evolutionary biology recognises the importance of networks of genes, and that fixating on single beneficial or deleterious mutations is trivialising evolution. The developmental biologist Paul Myers makes this clear:

Mutations are the root of biological variation, of course, but we often have a naive view of their consequences. Most mutations are neutral. Even advantageous mutations are subject to laws of chance in their propagation, and a positive selection coefficient does not mean there will be an inexorable march to fixation, where every individual has the allele. This is also true of deleterious mutations: chance often dominates, and unless it is a strongly negative allele, like an embryonic lethal mutation, there's also a chance it can spread through the population.
Stop thinking of mutations as unitary events that either get swiftly culled, because they're deleterious, or get swiftly hauled into prominence by the uplifting crane of natural selection. Mutations are usually negligible changes that get tossed into the stewpot of the gene pool, where they simmer mostly unnoticed and invisible to selection. Look at human faces, for instance: they're all different, and unless you're looking at the extremes of beauty or ugliness, the variations simply don't make much difference. Yet all those different faces really are the result of subtly different combinations of mutant forms of genes.
"Combinations" is the magic word. A single mutation rarely has a significant effect on a feature, but the combination of multiple mutations may have a detectable or even novel effect that can be seen by natural selection. And that's what's going on all the time: the population is a huge reservoir of genetic variation, and what we do when we reproduce is sort and mix and generate new combinations that are then tested in the environment. [32]

It can be quite difficult to get this simple point across – really serious mutations tend to kill in utero. Even then, some deleterious mutations can be beneficial in some environments, as the persistence of sickle cell anaemia in malaria-endemic areas demonstrates.

Thinking in terms of networks of genes helps realise the fallacy behind the “mutations are deleterious therefore evolution can’t occur” fallacy. Myers again:

The curious thing is, though, that the more elaborate the network, the more pieces tangled into the pathway, the smaller the effect of any individual component (in general, of course). What we find over and over again is that many mutations to any one component may have a completely indetectable effect on the output. The system is buffered to produce a reliable yield.
Now do you see what's wrong with the simplistic caricature of evolution at the top of this article? It's superficial; it ignores the richness of real biology; it limits and constrains the potential of evolution unrealistically. The concept of evolution as a change in allele frequencies over time is one small part of the whole of evolutionary processes. You've got to include network theory and gene and environmental interactions to really understand the phenomena. And the cool thing is that all of these perspectives make evolution an even more powerful force.

Abel’s argument is based on a parody of evolutionary theory, as well as an appalling level of ignorance of the primary literature, not to mention the confused definition of evolution with which he worked.

Conclusion

Abel's suggested strategy to help Christadelphian evolution denialists rebut evolution is hopelessly dated, based on a confused understanding of what mainstream biologists mean by evolution, and deeply indebted to special creationist arguments which were recognised as being wrong in the second half of the 20th century. Anyone using Abel's strategy will find that as John Morris (in a 2009 article attacking evolution!) admitted:

The trouble is, in trying to answer an ‘expert’, we can so readily be wrong-footed. Few of us have advanced qualifications in the relevant sciences, and if we fail to hold our own in discussions about fossils, for example, or if we reveal our ignorance of current molecular biology, we shall be deemed to have lost the contest! [33]

 The tragedy of course is that if a believer has been primed to think in terms of evolution versus creation, losing an exchange with a knowledgeable opponent will quite likely precipitate a crisis of faith. The sooner tired anti-evolution arguments such as those made in Wrested Scriptures are buried for good, the better for the intellectual health of our community.

References

1. The following section is taken from this BEREA Portal article with permission of the author

2. Coffin JM “Evolution of Retroviruses: Fossils in our DNA” Proceedings of the American Philosophical Society (2004) 148:3, 264-280

3. Johnson WE Coffin JM Constructing primate phylogenies from ancient retrovirus sequences Proc. Natl. Acad. Sci. USA (1999) 96:10254-10260

4. ibid p 10254
5. ibid p 10255
6. loc cit
7. Johnson WE Coffin JM op cit p 10255-10256
8. ibid p 10256
9. ibid p 10259

10. loc cit

11. The following section is taken from this BEREA Portal article with permission of the author

12. Franceschini G, Sirtori CR, Capurso A, et al. A-I Milano apoprotein: decreased high density lipoprotein cholesterol levels with significant lipoprotein modifications and without clinical atherosclerosis in an Italian family. J Clin Invest. 1980;66:892–900.
13. Sirtori C.R. et al “Cardiovascular Status of Carriers of the Apolipoprotein A-IMilano Mutant” Circulation. 2001;103:1949-1954.
14. Shah P.K. et al “High-Dose Recombinant Apolipoprotein A-IMilano Mobilizes Tissue Cholesterol and Rapidly Reduces Plaque Lipid and Macrophage Content in Apolipoprotein E–Deficient Mice” Circulation. 2001;103:3047-3050.
15. Stevens J.C. et al “Dating the origin of the CCR5-Delta32 AIDS-resistance allele by the coalescence of haplotypes.” Am J Hum Genet. 1998 Jun;62(6):1507-15.
16. Ohno S “Birth of a unique enzyme from an alternative reading frame of the preexisting, internally repetitious coding sequence” Proc. Natl. Acad. Sci. USA (1984) 81:2421-2425
17. Blount Z.D., Borland C.Z., Lenski R.E. "Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli" Proc. Natl. Acad. Sci. USA 2008 105:7899-7906
18. Thornton J.W. "Evolution of vertebrate steroid receptors from an ancestral estrogen receptor by ligand exploitation and serial genome expansions" Proc. Natl. Acad. Sci. USA (2001) 98:5671-5676
19. Bridgham J.T., Carroll S.M., Thornton J.W. “Evolution of Hormone-Receptor Complexity by Molecular Exploitation” Science (2006) 312:97-101
20. Fraser J.A. et al "Chromosomal Translocation and Segmental Duplication in Cryptococcus neoformans" Eukaryotic Cell (2005) 4:401-406
21. Kellis M, Birren B.W, Lander E.S. “Proof and evolutionary analysis of ancient genome duplication in the yeast Saccharomyces cerevisiae” Nature (2004) 428:617-624
22. Meyer A, Schartl M "Gene and genome duplications in vertebrates: the one-to-four (-to-eight in fish) rule and the evolution of novel gene functions" Curr Opin Cell Biol 1999, 11:699-704
23. Mi S et al "Syncytin is a captive retroviral envelope protein involved in human placental morphogenesis" Nature (2000) 403:785-789
24. McAdams H.H. Srinivasan B, Arkin A.P "The Evolution of Genetic Regulatory Systems in Bacteria" Nat Rev Genet (2004) 5:169-178
25. Lenski R.E., Ofria C, Pennock R.T., Adami C “The evolutionary origin of complex features” Nature (2003) 423:139-144
26. Nachman, M.W., Crowell, S.L. Estimate of the mutation rate per nucleotide in humans. Genetics 2000 156(1): 297-304.
27. Burke M.K., Rose M.R., “Experimental evolution with Drosophila” Am J Physiol Regul Integr Comp Physiol 296:R1847-R1854, 2009
28. ibid, p R1847
29. ibid, p R1849
30. loc cit.
31. Dobzhansky, T, Pavlovsky, O "An experimentally created incipient species of Drosophila", 1971 Nature 23:289-292.
32. Myers PZ “It’s more than genes, it’s networks and systems.” Pharyngula July 24th 2010. Accessed 27th Oct 2013.

33. Morris J "Darwin or the Gospel" The Christadelphian, November 2009