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.
