If the genomic evidence allows us to trace the line from modern humans back to ancient humans, just how far back can the evidence take us? It’s one thing to match DNA between modern and ancient humans when viable samples of DNA are found, but just how does genomic or genetic evidence allow us to trace ancestors and even transitions between species when we can’t sample the original DNA?
The short version of the answer is, “We can go back millions of years because of the information encoded in DNA”. The longer version of the answer takes some explaining, but it’s extremely interesting. The information contained in DNA has enabled molecular biologists to construct a model called the ‘universal tree of life’, mapping the continuity of succession from the original forms of life that are ancestral to all organisms, to every species now living on earth.1
To explain how this is possible, consider the verse below:
“The heavens declare the glory of God, andthe sky abovepro claims cdfrzs hhd his hindrowka handiwork.”
This verse from Psalm 91 (with its errors) is unique to this publication. The chances of this verse plus the errors – consisting of just 99 characters – ever appearing in another book are so remote, that they are virtually non-existent. The possibility of that exact sequence being composed anew by another author is simply too unrealistic to consider. Therefore, if that sequence of 99 characters ever appears in another book it’s because it was copied from this one. There is no other feasible explanation.
It’s the same with certain genetic sequences. They have acquired mutations that are so identifiable that the only way they could possibly exist in different species, is because they were copied from a common source – a common ancestor. That is the essence of how we are able to trace common ancestry across seemingly diverse species, but naturally there is more detail to it than that.
Genomic evidence for common descent: Pseudogenes
As their name would imply, pseudogenes resemble genes, but they are no longer able to encode proteins. They are dysfunctional versions of genes that are known to be functional in other species (or sometimes even in the host organism if duplicates occur).
If we were to consider that corrupted version of Psalm 91:1 above to be a “pseudo-verse” then it would be a very similar analogy for a pseudogene; i.e. a gene was once functional, but through a variety of reasons (such as a crippling mutation or duplication) has now become non-functional.
On this page, we won’t go into the details of the reasons as to how pseudogenes are formed, but for those who are interested in exploring this further, Daniel Fairbanks’ book Relics of Eden: The Powerful Evidence of Evolution in Human DNA is well worth a read.2 For those who want to explore deeper still, Graeme Finlay’s book Human Evolution: Genes, Genealogies and Phylogenies is also worth the read.3 The point that’s relevant for this discussion is the story told by these pseudogenes.
If a functional gene develops a mutation that affords the organism an advantage (for example a thicker shell or a darker fur) then that mutation would continue to be passed on to subsequent generations. Conversely, if a mutation had a negative consequence then it would be fatal or at least detrimental to the host. Quite probably over time this detrimental expression would die out of the population and we would lose any record of the mutation. But this applies to functional genes…
In the case of non-functional genes (pseudogenes) any mutation that occurs in these will have no adverse effects on the organism. As a result, pseudogenes have become a very useful record allowing us to trace ancestry through literally thousands of generations. (Remember there are just 300 generations between us and Adam and Eve.)
There are over 6,000 pseudogenes in the human genome, but one of the more widely known examples is that of the GULO-P pseudogene. In humans, chimpanzees, orangutans and macaques the gene is broken in exactly the same way, something that is only plausible if they share a common ancestor.4 Interestingly, guinea-pigs also have a non-functional GULO gene, but it was inactivated in a completely different way, which shows a separate mutation event that occurred.
The effect of this gene being broken is that humans, chimpanzees, orangutans, macaques and guinea-pigs are not able to synthesise their own vitamin-C. So although it could be considered a disadvantageous mutation, those species that cannot produce their own vitamin-C have been able to obtain it through their diet.
Genomic evidence for common descent: Endogenous Retroviral Elements
While elements like pseudogenes are created from the organism’s own genes, Endogenous Retroviral Elements (ERVs) are genetic fragments that became integrated into the organism’s germ line and passed down to its subsequent generations. Retroviruses are a group of RNA viruses which insert a DNA copy of their genome into the host cell in order to replicate. The chances that the same retrovirus would have become inserted into the genome of different species in exactly the same location is remarkably remote.
For example, the human and chimpanzee genomes are of a very similar length, and so the chances of an ERV inserting itself into the same place are between those species are about 1 in 3 billion. Add a third and fourth species to that and the odds of this occurring by chance make it virtually impossible.5 This is just one of the reasons we know that humans, chimpanzees and other great apes share a common ancestor.
Genomic evidence for common descent: Transposons
Transposons are very similar to viruses, but cannot cross cellular boundaries like viruses and so they only replicate within the genome of the host organism. Thus, for the purposes of this discussion we can consider transposons to be much like ERVs, except that they originate from somewhere within the host’s genome and have inserted copies of themselves elsewhere within the genome.
There is growing evidence that transposons can lead to diseases associated with genetic mutations, especially if they are inserted into regions of genes that regulate gene activity. For example, if the insertion were to occur in an area that inhibits activity thus restricting the inhibition, it would result in over-activity of genes. This can cause certain cancers, cell dysfunction, and other diseases such as haemophilia and muscular dystrophy.
Genomic evidence for common descent: Synteny
This term is used by biologists to describe the scenario when genes are arranged in the same order and orientation along chromosomes of different species. An order usually inherited from a common ancestor. Now that biologists have mapped the genomes of so many species, there is indisputable proof of synteny and common descent. Organisations such as Answers in Genesis and the Institute for Creation Research have repeatedly tried to poke holes in this but to no avail. It’s like trying to argue that different versions of the Bible are not related when we know they all have the same common ancestor in the original texts.
Synteny between genomes is interesting because in biological terms, there’s no need for genes to be the same order. Fruit flies have been used in many genetic experiments because they are very easy to breed. It has been noted that different species of fruit flies have quite different gene orders and chromosome structures, and yet they all are healthy and perfectly functional organisms.
Likewise, populations of mice with very different chromosome arrangements have also been shown to arise very rapidly in nature.
Psalms and sonnets
To illustrate these points with an analogy: It would be equivalent to finding a set of 1,000 bibles with spelling mistakes (SNPs), entire chapters corrupted in the same manner (pseudogenes), and Shakespearean sonnets inserted at random locations (ERVs), and verses randomly duplicated in different locations (transposons)…. And then finding another set somewhere else with the identical characteristics across billions of characters of text.
The odds of identical ‘mutations’ occurring across multiple collections are simply not worth even trying to calculate. The only plausible answer is that these collections are copies.
Likewise, when we look across the genomes from a variety of species and we see identical mutations in identical locations, the only plausible answer is that they share a common ancestor. Biologists have been able to demonstrate that many species are genetically related by comparing the sequence and location of pseudogenes, endogenous retroviruses, and transposons.
Likewise, someone not familiar with genetics or genomics is quite entitled to ask how we know that these sequences being identified are DNA sequences of other species. Without trying to be flippant about the answer: to someone who speaks “fluent Genome”, it’s like finding a Shakespearean sonnet in the middle of the Psalms. It’s so easily identified, and yet so out of place!
Reiterating the point…
In the last chapter, we acknowledged the elephant in the room, and discussed that whilst humans have not descended from today’s apes or monkeys, there is a common ancestor between us. We also considered some of the methods used to compare genomes.
Let’s explore this little further by looking at evidence that modern humans and modern chimpanzees share a common ancestor. Just to reiterate the point, this does NOT mean humans evolved from chimpanzees, but there are a number of identifiable sequences in our respective genomes that show there was a common ancestor between us.
Sequencing the human genome was successfully completed in April 2003. Shortly thereafter (in September 2005) the genome sequence of the chimpanzee was published, and comparisons showed that the two genomes were nearly identical. Since then, much has been spoken about the shared DNA between humans and chimps because the chimp genome is the closest to ours. Most scientists agree that that the human-chimp split occurred roughly 6 million years ago. One may well argue “of course there is shared DNA – did the Creator not use the same building blocks?”
Yes, he did – and that’s the point. Well, some of the point. We also need to consider this: In that shared DNA there are functional and non-functional genes (pseudogenes). That both genomes contain similar functional genes is perfectly understandable, because they are the building blocks. But we have to find a reason as to why both genomes also include identical non-functional or broken genes?
Just to illustrate this point, we can consider two further examples. In his book Evolving: The Human Effect and Why it Matters, biologist Daniel Fairbanks discusses a particular sequence called MT2P1.6 To describe this VERY briefly, there are viruses that use RNA as their genetic material. These are called retroviruses. Sometimes, when they infect a cell, the virus’s RNA is copied back into the cells’s DNA. In humans, they are call human endogenous retroviruses – or HERVs for short (this is what we looked at few chapters ago).
If these happened in functional genes, they would disrupt the functioning of the gene and this would have a negative outcome. However, when these happen in non-functional genes there is no negative effect, and so they become “stuck” in our genome as non-functional relics. The human genome has about 443,000 of these.
MT2P1 is a pseudogene, a broken relic. It serves no purpose because it is a non-functional sequence within a non-functional gene. If one tried to express this gene, there is simply nothing that can be produced. It is completely useless and harmless. However, it has remained in the genome and has been copied and passed on and on over time.
The MT2P1 pseudogene is found in exactly the same place in humans and in chimps. Therefore, the question that needs to be answered is this: If God created man from scratch with a fresh new genome, why would God place a non-functional remnant of RNA/DNA from chimps into humans – in exactly the same place?
To consider another example: In a paper entitled Genesis and the Genome, Denis Venema discusses another example of a pseudogene – that of the vitellogenin gene, associated with yolk production in egg-laying vertebrates such as fish, birds and even the platypus.7 The point he makes is that if placental mammals are indeed descended from egg-laying ancestors, then remnants of the vitellogenin gene sequence should exist in their genomes in the form of a pseudogene. So biologists went looking for vitellogenin, first determining the location of the functional vitellogenin gene in the chicken genome, and then locating these genes in the human genome, but obviously in a non-functional state.
Now, as one would expect in the case of common ancestry, the gene that was present in the human genome is also present in other genomes (such as the chimpanzee genome at the same precise location)8, the same modifiers making them non-functional.
Whilst the MT2P1 and vitellogenin pseudogenes are interesting, they are just two examples of thousands that exist with identical inactivating mutations shared between humans and chimpanzees.7
It all comes down to this…
The critical point is this: Can we prove that humans are an independent species, completely unrelated to all others? The simple answer is no, we can’t. We have the same genetic scars, the same broken sequences, the same identifiers. For example, in the case of the vitellogenin gene, the question begs asking as to why God would create man as a distinct new species, and yet include a non-functional yolk-making gene in our genome.
This is the reality we must face. If we had been created independently of other species, then we would have a ‘clean’ or unique genome. But we don’t. Our human genome is built upon the those of species that have gone before us, and this has been proven.
It doesn’t change the miracle of life. It doesn’t change the beauty of creation. I argue it has made God’s creative effort more spectacular whilst demonstrating how his intent came to fulfilment in humankind; and the evidence shows that to deny this is potentially to deny God’s creative craftsmanship.
To bring these points together…
In this chapter we have briefly described the various types of genetic phenomena that help to trace common ancestry. If you would like to investigate these in more detail then there are a number of excellent books available. We have already mentioned Daniel Fairbanks’ Relics of Eden, but others include:
- Francisco Ayala, “Darwin’s Gift: To Science and Religion”;
- Daniel Harrell & Tony Jones, “Nature’s Witness: How Evolution Can Inspire Faith”;
- Darrel R. Falk, “Coming to Peace with Science: Bridging the Worlds Between Faith and Biology”;
- Karl W. Giberson, Francis Collins, “The Language of Science and Faith: Straight Answers to Genuine Questions”; and
- Dennis Venema & Scott McKnight, “Adam and the Genome”.
1 Francisco Ayala, The Big Questions: Evolution (Quercus Publishing, 2012) eBook loc 236
2 Daniel Fairbanks, Relics of Eden: The Powerful Evidence of Evolution in Human DNA (Prometheus Books, 2007)
3 Graeme Finlay, Human Evolution: Genes, Genealogies and Phylogenies (Cambridge University Press, 2013) https://goo.gl/u7EIvW
4 Ken Gilmore, The Genomic Evidence for Common Descent: 3. Shared identical pseudogenes (Evolutionary Creationism: A Christadelphian Perspective, November 2014) https://goo.gl/qExKpB
5 Ken Gilmore, The Genomic Evidence for Common Descent: 5. Endogenous Retroviral Elements (Evolutionary Creationism: A Christadelphian Perspective, Nov 2014) https://goo.gl/jbKvB7
6 Daniel Fairbanks, Evolving: The Human Effect and Why it Matters (Prometheus Books, 2012)
7 Dennis Venema, Genesis and the Genome: Genomics Evidence for Human-Ape Common Ancestry and Ancestral Hominid Population Sizes (Perspectives on Science and Christian Faith, September 2010) Vol 62:3 P167