Evolution Basics: The Placental Revolution, Part 2

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December 12, 2013 Tags: Genetics, History of Life

Today's entry was written by Dennis Venema. You can read more about what we believe here.

Evolution Basics: The Placental Revolution, Part 2
Photo credit: Dallas Krentzel (Creative Commons Attribution 2.0 Generic)

Note: This series of posts is intended as a basic introduction to the science of evolution for non-specialists. You can see the introduction to this series here. In this post we discuss the earliest-known primate, and a chance event that would saddle some primate groups (including our own species) with the inability to synthesize their own vitamin C.

In the last post in this series, we examined the rapid diversification of placental mammals following the extinction of non-avian dinosaurs (caused by the asteroid impact marking the Cretaceous – Paleogene boundary 66 million years ago). Not long after this event (geologically speaking), primates enter the fossil record. Given that our own species is nested within the primates (a fact first recognized by Linnaeus in the 1700s), the origin of this group has been of considerable interest to paleontologists.

Presently, the oldest-known primate is a tiny creature from the middle Paleogene of what is present-day China. This tiny primate, Archicebus achilles, is a crown-group haplorhine, that lived about 55 million years ago. Haplorhines are a monophyletic group that includes present-day tarsiers, and anthropoid (or “human-like”) species: New - World monkeys, Old – World monkeys, and great apes - including humans. Tarsiers and anthropoids are more closely related to each other than to lemurs, another primate group with present-day species:

 

Phylogeny diagram

Phylogenetic relationships among crown-group primates, showing the position of the Archicebus achilles as a stem-group tarsier close to the base of the primate tree.

Beyond its age and current status as the oldest-known primate, Achicebus achilles is also noteworthy in that it appears to be very close to the last common ancestral population of the crown-group tarsier and crown-group anthropoid lineages, though it appears more closely related to tarsiers than to the anthropoid lineage (i.e. despite being close to the last common ancestor of tarsiers and anthropoids, Archicebus is best understood as a stem-group tarsier). The features of Archicebus and its location close to the base of the primate lineage suggest that last common ancestral population of primates was similarly small in stature, arboreal (tree-dwelling), and fed on insects. The location of Archicebus also supports the hypothesis that primates first evolved in Asia, and later migrated to Africa (where, as we will see in an upcoming post, the lineage leading to humans would evolve).

Goodbye to GULO

It is at the base of the haplorhine tree that an event occurs that we have previously discussed as strong evidence for human – ape common ancestry, and an event that many Christians who have examined the evidence for evolution are familiar with.  One shared feature of haplorhine primates is their curious inability to make their own vitamin C, forcing them to acquire it from their diet. This is unusual – the majority of mammals (including non-haplorhine primates) are able to make vitamin C starting from the basic dietary sugar glucose. The genetic reason for this deficiency has been determined: in haplorhine primates, the enzyme that performs the last step in vitamin C biosynthesis (called L-gulonolactone oxidase; abbreviated as “GULO”) is missing. Despite this lack of enzyme function, however, the mutated remains of the gene that codes for the GULO enzyme is found in these primates. Since this deficiency affects all haplorhine primates, the simplest explanation is that this enzyme function was lost only once, prior to the divergence of the haplorhine crown group:

 

Phylogeny diagram

In order to appreciate the molecular details of the loss of GULO in the haplorhine lineage, let’s briefly review gene structure and function, something that I have discussed in more detail elsewhere:

 

Genes have a typical structure (obviously simplified here somewhat). First off, there is the actual DNA sequence that specifies the protein product sequence (the so-called “coding sequence”, shown in blue). This sequence is usually broken up into segments in mammalian genes, and these sequences are spliced together when the DNA sequence of the gene is transcribed into a “working copy” called mRNA – a short duplicate of the code that can be used by the cell’s machinery to actually build the specified protein.

Gene structure diagram

The technical name for a gene segment that is spliced into the mRNA is an “exon” – and functional GULO genes in mammals have twelve exons. When comparing the sequence of the GULO gene in great apes (which are crown-group haplorhines), we see that many of the exons of the GULO gene have been deleted entirely, completely removing the possibility of function. In humans, for example, only exons 4, 7, 9, 10, and 12 remain – and chimpanzees and macaques have the same pattern:

 

GULO gene diagrams

A schematic diagram of a functional GULO gene compared to the state observed in several crown-group haplorhines for which genome sequence data is available. The same seven exons in humans, chimpanzees, and macaques are deleted from the GULO pseudogene, destroying the function of the enzyme.

It is not likely that all of the deletion events that removed these exons were the original mutations that removed the function of this gene in the haplorhine lineage. Rather, these deletions likely took place after the original loss of GULO function, when additional mutations to this (now nonfunctional) sequence would have no further consequence to an already defective gene. The shared deletions we see in great apes, however, did take place before these species went their separate ways – and were inherited by the resulting species in this group, in exactly the way we have discussed previously in this series, when we spent several posts likening genomes to “copied texts” that accumulate errors over time.

Shared mutations – a perennial challenge to antievolutionary views

While observing defective genes with identical mutations in nested groups of species is easy to understand from an evolutionary viewpoint, this issue remains an extremely difficult problem for antievolutionary organizations to explain. Indeed, the only recourse is to try to argue that the identical mutations we observe across numerous species were not inherited from a common ancestor – and thus must have occurred independently in each species. The probability of identical mutations occurring multiple times in independent species is of course vanishingly small, to say nothing of such events producing the precise phylogenetic pattern predicted by all other lines of evidence.

So, despite the unfortunate loss of GULO – and a consequent requirement for dietary vitamin C – the anthropoid lineage would continue to expand and diversify. In the next post in this series, we’ll continue to examine the diversification of this group, and the appearance of our own group within it: Homo.

For further reading


Dennis Venema is Fellow of Biology for The BioLogos Foundation and associate professor of biology at Trinity Western University in Langley, British Columbia. His research is focused on the genetics of pattern formation and signalling.

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