Sunday, 8 July 2018

The genetic scars of our insect-eating, egg-laying past - the powerful genomic evidence of common descent

The earliest mammals are believed to have been insect-eaters, which means that they would have had the genes for chitinase, an enzyme that digests chitin, the polysaccharide which is the main component of insect exoskeletons. Given this, common descent would predict that non-insectivorous mammals, which no longer need to digest chitin, would no longer have functioning chitinase genes, but instead have chitinase pseudogenes as inherited remnants of their insect-eating past.

Recently, Christopher Emerling, Frédéric Delsuc, and Michael Nachman published a paper in Science Advances in which they showed that in all the carnivorous and herbivorous animals whose genomes they examined, they found not only chitinase pseudogenes, but in animals previously known to share common ancestry, they found exactly the same mutations in some of the chitinase pseudogenes.

Regular readers of the website will be well-aware of the power of this argument; shared identical genomic 'errors', be they pseudogenes, endogenous retroviral elements, or retrotransposons are some of the strongest lines of evidence confirming common descent. Just as shared identical sections in exam papers confirm copying and cheating in students (identical independent errors are of course so unlikely an explanation as to be readily dismissed out of hand), so do shared identical genetic errors confirm the inheritance of a 'broken' genomic elements from a common ancestor of the species examined.

Similar evidence can be found from examples such as broken egg yolk protein genes in placental mammals, broken olfactory receptors in aquatic mammals such as whales, broken tooth-enamel genes in toothless animals, and the broken vitamin C synthesising gene GULO in humans and primates. These previously-mentioned examples made the case for common long ago, but papers such as this are invaluable if only to show the power of evolutionary theory in its ability to make predictions, and explain facts.

Emerling et found that instead of one CHIA gene, there were five paralogous genes, consistent with duplication from a single ancestral CHIA gene:
Phylogenetic analyses cluster these into five major clades... which we refer to as CHIA1, CHIA2, CHIA3, CHIA4, and CHIA5. All four superorders of placental mammals (Xenarthra, Afrotheria, Euarchontoglires, and Laurasiatheria) are represented by orthologs in all five CHIA clades, implying that the last common ancestor of placental mammals had five CHIAs. [1]
The image below shows the distribution of the CHIA genes in the placental mammal divisions, with pseudogenes represented by open circles and functioning genes by closed circles:

Phylogeny showing the similarity between the different chitinase genes (closed circles) and pseudogenes (open circles). Colors and silhouettes correspond to different groups of mammals.

Two things are apparent. The first is that organisms that are not primarily insectivorous such as humans can have a functioning chitinase gene. This suggests the possibility that a CHIA gene has achieved a secondary function [2] in the line leading to the organism, meaning that even when the diet shifted from insectivory, that gene was conserved by selection. The second is that there is a strong correlation between number of CHIA genes and insects as a percentage of diet:

Number of functional contig-derived CHIAs versus the percent of the diet consisting of invertebrates.

As the authors state, this correlation between insectivory and CHIA gene number, allows us to infer that the ancestor of placental mammals had the five CHIA genes CHIA1 through CHIA5, something which agrees well with the fossil evidence which shows that the earliest placental mammals were shrew-like, insectivorous animals. [3] While a special creationist could plausibly argue that if an animal's diet has a higher proportion of insects, then it would have been created with more copies of CHIA to better facilitate chitin digestion, it is the presence, distribution, and patter of disabling mutations in clades that yet again poses a huge challenge for special creation, while being entirely consistent with common descent.

The timing and distribution of the CHIA gene loss of function as the authors note corresponds to the diversification of herbivorous and carnivorous lineages in the mammalian adaptive radiation after the dinosaur extinction event:

Significantly, all or nearly all CHIA genes were lost during the origin and diversification of noninsectivorous lineages, including the herbivorous sloths (Folivora), hyraxes, elephants, and sirenians (Paenungulata), Old World fruit bats (Pteropodidae), horses, rhinoceroses, and tapirs (Perissodactyla),  camels, swine, and ruminants (Cetartiodactyla), colugos (Dermoptera), lemurs (Lemuriformes), monkeys and apes (Anthropoidea), rabbits and pikas (Lagomorpha), rodents (Rodentia), and the largely carnivorous false vampire bats (Megadermatidae), whales (Cetacea), and dogs, cats, and kin (Carnivora). [4]
This of course makes sense when you realise that carnivorous and herbivorous placental mammals would not miss the loss through mutation or deletion of CHIA genes, and that such losses would occur around those times. Again, under a model of special creation, one would simply not expect to see broken CHIA genes in non-insectivorous mammals if each species was specially created. Conversely, this is exactly the sort of thing we'd expect to see if placental mammals shared a common insectivorous ancestor with five CHIA genes, with some or all of those CHIA genes becoming pseudogenes in lineages shifting towards herbivorous or carnivorous diets.

 Patterns of CHIA gene loss through time

The really fascinating part of this paper is the discovery of patterns of the same inactivation in CHIA pseudogenes in groups of modern mammals that share common ancestry, entirely consistent with that inactivating mutation occurring in the common ancestor of those mammals. As Emerling points out at his website:

What’s more is that many of these mammals that are thought to be related, based on DNA and anatomical similarity, share the exact same mutations in some or all of the chitinase genes. For example, horses and rhinos look quite different from one another, yet have been considered by anatomists, paleontologists and geneticists to be related for over a century and a half. They are both herbivores, which implies their diet was inherited from a common ancestor, and indeed the earliest fossils that resemble them had teeth and jaws that appeared to be particularly good at eating plants. Such adaptations would have rendered insect-digesting genes relatively useless. Indeed, horses and rhinos have pseudogene remnants for four of the five chitinases, and they share at least one disabling mutation in each gene, suggesting they inherited defunct copies from a plant-eating ancestor.

Humans also possess three chitinase pseudogenes, alongside a single functional chitinase gene. Two of the pseudogenes share the same inactivating mutations with monkeys and apes, and a third shares a mutation only with apes. Interestingly, many of the earliest primate fossils appear to have been insect-eaters, but as monkeys and apes appeared, plants, as well as meats, became more important for their diets, so insect-digesting genes were likely less useful.

Together, these data suggest that in our very own genomes, we retain ‘molecular fossils’, that hearken back to a time when our distant ancestors were not the top of the food chain, but rather scurried along amidst dinosaurs, eating insects. [5] (Emphasis mine)

Examples of CHIA shared inactivating mutations.

The authors note that there are some discrepancies in the data that indicate the need for more research, such as mismatch between diet and CHIA gene number, such as one sees with the baleen whale Balaenoptera acutorostrata which has only one CHIA gene despite the fact its diet is rich in crustaceans whose exoskeletons are rich in chitin. The authors quite plausibly state that this may well be an example of contingency in evolution, where CHIA loss occurred in the terrestrial ancestors of whales, meaning that when they began their shift in diet towards chitin-rich crustaceans, they simply did not have the full complement of CHIA genes to exploit. [6] Other discrepancies are harder to explain, once again indicating the need for further research into this problem. However, as the authors note in their conclusion:
Together, these results suggest that chitinase genes (CHIAs) provide a genomic signal of the post-K/Pg dietary radiation of placental mammals. Consistent with the fossil record, the patterns of CHIA evolution indicate that the earliest placental mammals were highly insectivorous and that descendant lineages adapted to noninsectivorous dietary niches near and after the K/Pg boundary. Consequently, many placental mammals, including humans, retain “genomic fossils” in the form of CHIA pseudogenes, providing a molecular record of their insectivorous past. [7] (Emphasis  mine)
Both the shared identical mutations in CHIA pseudogenes in groups of mammals regarded as having common ancestors, and the congruence between the fossil record of insectivory in early placental mammals and the genomic data are exactly what common descent would predict. Conversely, there is simply no credible special creationist answer. As Emerling, who professes religious faith notes at his blog:

Why would the Creator design humans, rhinos, tigers and other mammals that never or almost never eat insects with remnants of insect-digesting genes? Is it just a coincidence that the earliest mammal fossils, found alongside dinosaurs, appear to have been insect eaters, and modern herbivores and carnivores have remnants of insect-digesting genes? For those that believe that all animals were plant-eaters in the Garden of Eden, why do so many herbivores have remnants of insect-eating genes? If mammals were created in the last 10,000–6,000 years, how could they evolve from insect-eaters to herbivores and carnivores so quickly, modifying their teeth, jaws, intestinal tracts, etc. to be optimized for their new diets? [7]
Why indeed. 


1. Christopher A. Emerling, Frédéric Delsuc, and Michael W. Nachman "Chitinase genes (CHIAs) provide genomic footprints of a post-Cretaceous dietary radiation in placental mammals" Science Advances 16 May 2018: Vol. 4, no. 5, eaar6478 DOI: 10.1126/sciadv.aar6478, p1
2. Emerling suggests, quite reasonably in my opinion, that in humans, the functioning CHIA gene has taken on an immune role to "to help protect the body from pathogenic fungi, since fungi have chitin in their cell walls" which would explain its activation in lung tissue.
3. Emerling, op cit, p2
4. ibid, p 2
5. Christopher Emerling "Genes suggest rhinos, tigers, humans and all other mammals had insect-eating ancestors" Evolution For Skeptics June 11, 2018
6. Emerling, Delusc, Nachman, op cit p 5
7. See ref. 5