I started this series by referring to an appallingly bad article in the January 2005 edition of The Testimony which tried to hand-wave away the considerable evidence for common descent from molecular genetics by trying to call it just another variation of the argument from comparative anatomy. Brief mention was made by the author - John Watts - of a paper by molecular biologist Graeme Finlay which covered the evidence for human evolution from molecular biology. Watts' coverage was non-existent - which made his dismissal of the paper yet another example of the intellectually dishonest way in which The Testimony has been covering science for some time. The following post will provide an overview of Finlay's paper.
Finlay outlines the evidence for human-ape common ancestry from molecular genetics:
(1) Our chromosomes have taken shape by familiar processes of cutting and pasting.(2) We share with other species uniquely rearranged genes.(3) We share with other species unique random additions to our DNA <1>
Finlay begins with the evidence that human chromosome 2 is a fusion of two chromosomes homologous to those found in great apes. The evidence for this is compelling, and is widely regarded as consistent with common descent.
High resolution cytogenetic mapping has shown how the chromosomes of the great apes (humans, chimps, gorillas, orangutans) may be rearranged to form an ancestral set. The structures of most of the chromosomes belonging to this common ancestor have been unambiguously derived. Blocks of human chromosomal material can be cut-and-pasted to give the chromosome sets of gibbons (lesser apes), macaques (Old World Monkeys) or ancestral primates. <2>
This, it needs to be stressed is entirely consistent with common descent, where not only the same genes, but the same order of genes in a common ancestor of primates is inherited, with inversions of syntenic blocks occurring after the lines from the ancestral species diverged. Watts needs to explain why God has created species that evolutionary biology say have a common ancestor with similar genes arranged in a similar order, complete with inversions of chromosome blocks that look exactly like inversion events.
The argument from common design founders when, as Finlay points out, we see common design flaws in closely related species. Finlay again:
Humans and chimpanzees (but not other primates) share duplicated chromosomal segments which have generated two copies of a novel gene, and produced the unstable ‘CMT’ genetic region involved in neurological diseases. These duplications must have been generated in a creature ancestral to humans and chimps. Another duplication inherited by humans, chimps, and gorillas is implicated in chromosomal instability giving rise to leukaemias. <3>
This is extremely difficult (to put it charitably) to reconcile with any theory of design, as one needs to explain convincingly why humans and chimps have the same duplicated chromosomal segments resulting in the same copy of a gene. This, as Finlay points out increases the risk of disease. The odds of humans and chimps having exactly the same chromosomal segment duplication by chance are remote. Arguing that it is a design feature is untenable since this genetic quirk increases the risk of disease. The only credible answer is that this duplication occurred in a common ancestor of humans and chimps and was subsequently inherited.
Finlay continues by showing that the human genome not only is littered with thousands of pseudogenes, but that humans, apes and monkeys share many pseudogenes in a pattern entirely consistent with common descent:
The argument for common descent based on shared pseudogenes is as the above shows not restricted to the GULO pseudogene, and as one can see, these pseudogenes appear in the order one would expect if they first appeared in a common ancestor of the affected primates and were subsequently inherited. Again, the odds of simultaneous pseudogenisation events occurring solely in primates and in a pattern that would purely by chance simulate common descent is extremely unlikely. As Finlay points out:
Some of these genetic fossils are found in humans and other species, and contain the same inactivating lesions in the different species. It is vanishingly unlikely that they would arise independently in two or more species. All the species that possess a particular genetic relic must have inherited it from a common ancestor in which the gene sustained its unique inactivating damage.
For example, the a-fucosyltransferase pseudogene is shared by humans, chimps, and gorillas31. A nucleotide triplet CAA (which specifies glutamine, ‘Q’) has mutated to TAA (a ‘stop’ signal, ‘*’):
gibbon, orang..................SPFDVVFRPQAAFLPEWVG…
human, chimp, gorilla..........SPFNVVFRP*
As a result of the mutation to a stop signal, the gene no longer encodes the complete a-fucosyltransferase enzyme. In a further example, humans, chimps, gorillas and orangutans have inherited the same scrambled endozepine-like peptide gene. This gene was destroyed in a great ape ancestor when an ‘A’ was inserted into the genetic sequence, obliterating the downstream protein sequence (‘xxxxx’).
macaque..........................ALKQLKGPVSDPEKLLIYG…
chimp, gorilla, orang............ALKQLKGTVCDQEKxxxxx…
human............................ALKQLKGTVCDQERxxxxx…
The urate oxidase gene was also inactivated in a great ape ancestor when a C to T (italicised) mutation generated a ‘TGA’ (‘stop’) signal (underlined).
four monkey species................ATTCAGCGAGATGGAAAATAT…
human, chimp, gorilla, orang.......ATTCAGTGAGATGGAAAATAT… <4>
Common design simply breaks down when it is applied to such data, as it is scarcely credible to argue that not only will an intelligent designer insert broken genetic material into the DNA of animals, but do so repeatedly in such a way as to simulate common descent. Postulating that these occurred purely by chance is an argument from desperation given the sheer improbability of these events repeatedly occurring in just the right way as to simulate common descent. The one explanation which consistently and readily explains the data is the fact that humans, apes and monkey share a common ancestor, and in the common ancestor of humans, humans and apes and humans, apes and monkeys respectively, pseudogenisation events occurred which were subsequently inherited.
Finlay spends some time (justifiably) on ERVs and retrotransposons as they provide the most powerful evidenced for common descent. He notes that over 40% of our DNA is retrotransposed material:
Reverse transcribed elements such as LINEs, SINES and processed pseudogenes are intracellular parasites that replicate within a single lineage of cells and are severely restricted in their ability to travel into the DNA of other species. Patterns of inheritance are not obscured by transmission as infectious agents. If one of these elements is inserted at the same site in the DNA of different species, then those species must have inherited that insert from the same ancestor. All the species containing the particular cassette are descendants of the one creature in which the unique insertion event occurred. <5>
What is clear is that these elements were not part of the original genome, but are the result of retrotransposition. ERVs in particular are alien to the host genome, being retroviral genetic material, so any theory of common design founders on the fact that not only are these retrotransposed elements, but foreign genomic material. As Finaly says, “Each unique provirus present in different species establishes that those species are descended from the ancestor in which the provirus spliced itself into the primate genome.” <6>
Finlay continues his presentation of the evidence for common descent from common retrotransposed elements by looking at LINEs (long interspersed elements) and SINEs (short interspersed elements). LINEs are short sections of DNA containing the enzyme reverse transcriptase and other genetic materials. They are able to make an RNA transcript of themselves, convert it to DNA and insert this randomly in the host genome. SINEs lack reverse transcriptase, and therefore are usually dependent on LINEs to provide the machinery of reverse transcription.
LINE and SINE insertion is usually harmless, and rarely beneficial if they are co-opted by the host genome for another function. However, they are linked with disease, so any creationist theory which argues that this is evidence for design needs to account for why such marginal benefit is accompanied by significant morbidity from non-innocuous retrotransposition insertion.
Again, the evidence for common descent for LINEs and SINEs comes from the fact that identical LINEs and SINEs are found in exactly the same place in genomes of related species, in such a way that would be consistent with their insertion in a common ancestor of those species. Finlay continues: <7>
Individual LINEs with the features of recent insertions are found in human DNA only. Other LINEs at unique sites which show slightly older characteristics are shared by humans and chimps, or by humans, chimps, and gorillas. Over 50 older LINEs have been identified that are common to the great apes.
The insertion of a SINE (such as an Alu cassette) into cellular DNA is rare and random. It is highly unlikely that the same SINE would insert independently into the same site in different species. Alu sequences are clear markers of evolutionary relationships.
groups with common Alu insert Alu location
great ape: pseudo-autosomal boundary, a-globin 2 gene
great ape, lesser ape: a-globin genes (six cassettes), ‘EPL’ locus
great ape, lesser ape, OWM: RHAG genes (three cassettes), FRG1 gene (two cassettes), interferon-g gene
great ape, lesser ape, OWM, NWM: RHCE blood group gene, blue opsin gene, BC200 gene
great ape, lesser ape, OWM, NWM, tarsiers: ATP synthase b gene, zonadhesion gene, a1-microglobulin gene
The insertion site of an Alu element common to the apes, OWMs and NWMs is provided as an example. This Alu element has resided in primate DNA since the simian common ancestor. The 16 nucleotides shown on each side of the Alu cassette represent the duplicated sequences identifying the unique insertion site.
insertion site.......................TAATAATACAACTTTT
human...................---AG---TG------[Alu]TAATAATACAACTTTT
chimpanzee..............---CG----G------[Alu]----------------
gorilla.................---CG----G------[Alu]----------------
orangutan...............---CG----G------[Alu]-------DDG------
gibbon..................---CG----G------[Alu]-D--------------
baboon (OWM)............----G---AG------[Alu]----------------
rhesus macaque (OWM)....----G---AG------[Alu]DDD------G------
barbary macaque (OWM)...----G---AG------[Alu]DDD------G------
marmoset (NWM)..........----------------[Alu]--D---C----A---
Finlay concludes his presentation by stating:
Arguments about evolution continue after 150 years. But the unique genetic markers reviewed above establish unequivocally the fact of our evolution. DNA markers called microsatellites are used for forensic purposes. They establish guilt or innocence, and resolve questions of paternity beyond reasonable doubt even though they are not unique markers like pseudogenes and retrotransposed sequences. The assertion that we have evolved is established beyond reasonable doubt. These findings must deal to the hermeneutic paradigm of biblical literalism what Galileo’s findings dealt to the Aristotelian paradigm of his day. <8>
By attempting to dismiss this as a variation of the argument from comparative anatomy, Watts has demonstrated that he simply has failed to understand the article. The unimaginably large coding space for genes means that every animal could code for proteins such as cytochrome c in such a way as to rule out common descent. Every living creature could have its genes arrayed in such a way as to minimise synteny to levels utterly inconsistent with common descent. Common design does not explain gene homology or high synteny in related species. Neither does it explain the presence of shared pseudogenes appearing in related species in a way consistent with the predictions of common descent. Nor can it explain shared retrotransposed elements, particularly shared ERV elements. This data is not contested outside of a tiny rump of fundamentalists whose arguments are based not on science, but on Biblical literalism. The fact that even believing molecular biologists such as Finlay accept the evidence shows common descent made it hard for Watts to dismiss this as an ‘atheistic’ reading of the data. What it does do however is show that the burden of proof is on the science denialists in our community to credibly explain this from a special creationist perspective.
References
1. Finlay G “Homo divinus: the ape that bears God’s image”. Science and Christian Belief (2003) 15:17
2. Coffin JM “Evolution of Retroviruses: Fossils in our DNA” Proceedings of the American Philosophical Society (2004) 148:3, 264-280
3. Finlay, p 22-23
4. ibid, p 25-26
5. ibid, p 27
6. ibid, p 28
7. ibid, p 28-29
8. ibid, p 32
3. Finlay, p 22-23
4. ibid, p 25-26
5. ibid, p 27
6. ibid, p 28
7. ibid, p 28-29
8. ibid, p 32
