Common Ancestry: An Introduction

A central tenet of evolutionary biology is the notion of common ancestry. The theory of descent with modification ultimately connects all organisms to a single common ancestor. Humans, butterflies, lettuce, and bacteria all trace their lineages back to the same primordial stock. The crucial evidence for universal common ancestry includes homology.

Why Common Ancestry Matters

Common ancestry is the conceptual foundation upon which all of modern biology, including biomedical science, is built. Because we are descended from the same ancestral lineage as monkeys, mice, baker’s yeast, and even bacteria, we share with these organisms numerous homologies in the internal machinery of our cells. This is why studies of other organisms can teach us about ourselves.
Consider work on mice and yeast by Kriston McGary and colleagues (2010) in the lab of Edward Marcotte. The researchers knew that because mice and yeast are derived from a common ancestor, we find not only many of the same genes in both creatures, but many of the same groups of genes working together to carry out biological functions—what we might call gene teams. The scientists thus guessed that a good place to look for genes associated with mammalian diseases would be on mouse gene teams whose members are also teammates in yeast. Using a database of genes known to occur in both mice and yeast, McGary and colleagues first identified gene teams as sets of genes associated with a particular phenotype. In mice the phenotype might be a disease. In yeast it might be sensitivity to a particular drug. The researchers then looked for mouse and yeast gene teams with overlapping membership.

Among the pairs of overlapping teams they found was a mouse team of eight genes known to be involved in the development of blood vessels (angiogenesis) and a yeast team of 67 genes known to influence sensitivity to the drug lovastatin. These teams formed a pair because of the five genes that belonged to both. The connection between the two teams suggested that both might be larger than previously suspected, and that more than just five genes might play for both. In particular, the 62 genes from the yeast lovastatin team not already known to belong to the mouse angiogenesis team might, in fact, be members. Starting with this list of 62 candidates, the researchers conducted experiments in frogs revealing a role in angiogenesis for at least five of the genes. Three more genes on the list turned out to have been identified already as angiogenesis genes, but had not been flagged as such in the researchers’ database. Eight hits in 62 tries is a much higher success rate than would have been expected had the researchers simply chosen genes at random and tested their influence on angiogenesis. In other words, McGary and colleagues used genetic data from yeast, an organism with neither blood nor blood vessels, to identify genes in mammals that influence blood vessel growth. Researchers in Marcotte’s lab have since exploited the overlap between the yeast lovastatin team and the mouse angiogenesis team to identify an antifungal drug as an angiogenesis inhibitor that may be useful

in treating cancer (Cha et al. 2012). That the theory of descent with modification is such a powerful research tool indicates that it has a thing or two going for it.

Homology 

As the fields of comparative anatomy and comparative embryology developed in the early 1800s, one of the most striking results to emerge was that fundamental similarities underlie the obvious physical differences among species. Early researchers called the phenomenon homology—literally, the study of likeness. Richard Owen, Britain’s leading anatomist, defined homology as “the same organ in different animals under every variety of form and function.”

Structural Homology

A famous example of homology comes from work by Owen and by Georges Cuvier, the founder of comparative anatomy. They described extensive similarities among vertebrate skeletons and organs. Referring to Owen and Cuvier’s work, Darwin (1859, p. 434) wrote:

What could be more curious than that the hand of a man, formed for grasping, that of a mole for digging, the leg of the horse, the paddle of the porpoise, and the wing of the bat, should all be constructed on the same pattern, and should include the same bones, in the same relative positions?

Figure 1

His point was that the underlying design of these vertebrate forelimbs is similar, even though their function and appearance are different.This makes the similarity in design among vertebrate forelimbs different from, say, that between a shark and a whale .Both shark and whale have a

streamlined shape, short fins or flippers for steering, and a strong tail for propulsion. These similarities in form make sense in view of their function: fast movement in water. Human engineers use the same features in watercraft. In contrast, the internal similarity between forelimbs with radically different functions seems arbitrary. Would an engineer design tools for grasping, digging, running, swimming, and flying using the same structural elements in the same arrangement? Darwin himself (1862) analyzed the anatomy of orchid flowers (Figure 2) and showed that, despite their diversity in shape and in the pollinators they attract, they are constructed from the same set of component pieces. Like vertebrate forelimbs, the flowers have the same parts in the same relative positions.

Figure 2

What causes these similarities in construction despite differences in form and function? Darwin argued that descent from a common ancestor is the most logical explanation. He argued that the orchids in Figure  are similar because they share a common ancestor. Likewise, the tetrapods in Figure 1 have similar forelimbs because they are descended from a single lineage, from which they inherited the fundamental design of their appendages.

Using Homology to Test the Hypothesis of Common Ancestry

We can use homologous traits shared among species to test Darwin’s hypothesis of common ancestry. We will show the logic using evolutionary novelties shared among imaginary snail species derived with modification from a single lineage. shows the evolutionary history. The common ancestor is the lineage of squat-shelled blue snails at far left. This lineage underwent speciation (1). One of the daughter lineages persisted to the present with no further changes in its shell (2). The other lineage evolved elongated shells (3). The lineage with elongated shells underwent speciation (4). One daughter lineage evolved bands on its shell (5), then persisted to the present with no further changes (6). The other daughter evolved pink shells (7), then split (8). One daughter lineage evolved high-spired shells (9). The other persisted with no further changes (10). The high-spired lineage split (11). One daughter lineage persisted with no further changes (12). The other evolved spikes on its shell (13), then persisted with no further changes (14). These events yielded the five extant species at far right. shows the novel shell traits shared by the four species that exhibit them. Note that these traits are shared in a nested pattern. The species with spikes is nested within the set of species with high spires. The set of species with high spires is nested within the set of species with pink shells. And the set of species with pink shells is nested within the set of species with elongated shells

Figure 3

Our hypothetical snails demonstrate that the theory of descent with modification from common ancestors makes a prediction. Extant organisms should share nested sets of novel traits. And, indeed, they do. For example, humans are nested within the apes—a group of species that have large brains and no tails. The apes, in turn, are nested within the primates—which have grasping hands, and feet, with flat nails instead of claws. The primates are nested within the mammals—defined by hair and feeding milk to their young. The mammals are nested within the tetrapods, the tetrapods within the vertebrates, and so on. The nested pattern of traits shared among extant species thus confirms a prediction of Darwin’s theory. But we can go further. Look again at Figure 3 and compare part (b) to part (a). Notice that the most deeply nested sets are defined by traits, such as spikes, that evolved relatively late. If we start with one of these sets and work our way out across the progressively larger sets that enclose it, we encounter additional traits that evolved ever earlier in time. Spikes were preceded by high spires. High spires, in turn, were preceded by pink shells. And pink shells were preceded by elongated shells. Even if we had only the five extant species and did not know their evolutionary history, we could still use the nesting of the traits they share to predict the order in which the traits should appear in the fossil record. We could then check the fossil record to see if our prediction is correct. Mark Norell and Michael Novacek (1992) performed such tests on two dozengroups of vertebrates. Representative results appear in. In six cases, such as the duck-billed dinosaurs, there was no significant correlation between the predicted order in which traits arose versus the actual order. However, in the other 18 cases, including the reptiles and the elephants and kin, the correlation was significant or strongly so.

More sophisticated methods of assessing the correspondence between traitbased reconstructions of evolutionary history versus the order traits appear in the fossil record have since been developed (see Wills et al. 2008). The correspondence is generally high, at least for well-studied groups of organisms that fossilize readily. This pattern is consistent with descent from common ancestors.

Molecular Homology

Figure 4

Curious similarities unrelated to functional need appear at the molecular level as well. Consider a genetic flaw on chromosome 17 in humans. Shared flaws are especially useful in distinguishing between special creation versus descent from a common ancestor. The reason is familiar to any instructor who has caught a student cheating on an exam. If A sat next to B and wrote identical correct answers, it tells us little. But if A sat next to B and wrote identical wrong answers, our suspicions rise. Likewise, shared flaws in organisms suggest common ancestry. The flaw on chromosome 17 sits near the gene for a protein called peripheral myelin protein-22, or PMP-22. The gene is flanked on both sides by identical sequences of DNA, called the CMT1A repeats Figure 4a. This situation arose when the distal repeat, which contains part of the gene for a protein called COX10, was duplicated and inserted on the other side of the PMP-22 gene (Reiter et al. 1997). The presence of the proximal CMT1A repeat has to be considered a genetic flaw because it occasionally lines up with the distal repeat during meiosis, resulting in unequal crossing over (Figure 2.28b; Lopes et al. 1998). Among the products are a chromosome with two copies of PMP-22 and a chromosome that is missing the PMP-22 gene altogether. If either of these abnormal chromosomes participates in a fertilization, the resulting zygote is predisposed to neurological disease (Figure 2.28c). Individuals with three copies of PMP-22 suffer from Charcot-Marie-Tooth disease type 1A. Individuals with only one copy of PMP-22 suffer from hereditary neuropathy with liability to pressive palsies. Motivated by the hypothesis that humans share a more recent common ancestor with the chimpanzees than either humans or chimps do with any other species, Marcel Keller and colleagues (1999) examined the chromosomes of common chimpanzees, bonobos (also known as pygmy chimpanzees), gorillas, orangutans, and several other primates. Both common chimps and bonobos share with us the paired CMT1A repeats that can induce unequal crossing over. The proximal repeat is absent, however, in gorillas, orangutans, and all other species the researchers examined. This result is difficult to explain under the view that humans and chimpanzees were separately created. But it makes sense under the hypothesis that humans are a sister species to the two chimpanzees. All three species inherited the proximal repeat from a recent common ancestor, just as three of the snail species in Figure 3 inherited pink shells.

 

A Predictive Test of Common Ancestry Using Molecular Homologies

Our second example of molecular homology concerns another kind of genetic quirk that might be considered a flaw: processed pseudogenes. Before we explain what processed pseudogenes are, note that most genes in the human genome consist of small coding bits, or exons, separated by noncoding intervening sequences, or introns. After a gene is transcribed into messenger RNA, the introns have to be spliced out before the message can be translated into protein. Note also that the human genome is littered with retrotransposons, retroviruslike genetic elements that jump from place to place in the genome via transcription to RNA, reverse transcription to DNA, and insertion at a new site (see Luning Prak and Kazazian 2000). Some of the retrotransposons in our genome are active and encode functional reverse transcriptase. Now we can explain that processed pseudogenes are nonfunctional copies of normal genes that originate when processed mRNAs are accidentally reverse transcribed to DNA by reverse transcriptase, then inserted back into the genome

Universal Molecular Homologies

Universal Triplet Code

The molecular homologies we have discussed so far have been confined to small numbers of species. Advances in molecular genetics have revealed, however, many fundamental similarities among organisms. Prominent among them is the genetic code. With minor exceptions (Knight et al. 2001), all organisms studied to date use the same nucleotide triplets, or codons, to specify the same amino acids to be incorporated into proteins. This is why genetic engineers can, for example, take the gene for green fluorescent protein from a jellyfish, transfer it into the fertilized eggs of a monkey, and get green fluorescent baby monkeys (Yang et al. 2008). Like the forelimbs in Figure 1, the genetic code appears highly evolved (Judson and Haydon 1999). The pattern of codon assignments to amino acids reduces ill effects of point mutations and translation errors (Freeland et al. 2003) and facilitates rapid evolution of proteins by selection (Zhu and Freeland 2006). Also like the forelimbs, however, many details of the code have clearly arisen as a result of something other than functional necessity. An enormous number of alternative codes are theoretically possible, some of which would work better than the real one (Koonin and Novozhilov 2009; Kurnaz et al. 2010). Furthermore, having a unique genetic code might offer distinct advantages. For example, if humans used a different genetic code from chimpanzees, we would not have been susceptible to the chimpanzee virus that jumped to humans and became HIV. When the virus attempted to replicate inside human cells, its proteins would have been garbled during translation.If alternative genetic codes are possible, and if using them would be advantageous, then why do virtually all organisms use the same one? Darwin provided a logical answer a century before the genetic code was deciphered: All organisms inherited their fundamental internal machinery from a common ancestor.