The natural world is rife with leftovers. Over the course of evolution, body parts that no longer benefit their owners eventually waste, away leaving behind shrivelled and useless anatomical remnants. The human tailbone is one such example. Others include the sightless eyes of cavefish that live in total darkness, the tiny spurs on boas and pythons that hint at the legs of their ancestors, and the withered wings of the Galapagos cormorant, an animal that dispensed with flight on an island bereft of land predators.
Animal genomes contain similar remains. Just like organs, genes also waste away if they stop being useful. They accumulate crippling mutations that kill their ability to make proteins and turn them into functionless “pseudogenes“. They have no useful role other than to tell inquisitive geneticists about their histories.
So organs can degenerate and genes can decay. The two processes should clearly run in parallel, but there are few documented examples of this. Robert Meredith from the University of California Riverside, has uncovered just such an example, a beautiful case study where the decay of a gene called enamelin clearly parallels the loss of a body part – tooth enamel.
Enamel is an extremely tough material that coats the outside of our teeth. Many proteins are essential for making it, including the aptly named enamelin, which is produced by a gene of the same name. Meredith’s team sequenced the enamelin gene (ENAM) in 20 species of mammals that either have teeth without enamel caps (like aardvarks, sloths and armadillos) or that lack teeth altogether (like anteaters, pangolins and several whales).
Today, every single one of these species has a broken version of enamelin. Mutations have crept into these genes, which stop the production of the protein before it’s fully formed. The result is a busted gene that produces a runty, useless protein. Other mammals don’t suffer from this problem; Meredith found that ENAM is fully functional in 29 other toothed mammals, including cats, cows and dolphins.
This is exactly what you’d expect, but the clear link between the lack of enamel and a broken enamel-producing gene is exciting nonetheless. It’s a tale that, in Meredith’s own words, provides “manifest evidence for the predictive power of Darwin’s theory”.
Our teeth are a mystery. The set we grow during late childhood stays with us throughout our lives, biting and chewing thousands of times a day. They can withstand forces of up to 1,000 newtons and yet, the material that coats them – enamel – is little tougher than glass. How does this extraordinarily brittle substance not shatter into pieces every time we crunch a nut or chomp on an apple?
Herzl Chai from Tel Aviv University found the answer, and it’s a surprising one. At a microscopic level, our teeth defend against fractures by developing with cracks already built in. These pre-made defects are known as “tufts” because of their wavy appearance. They are scattered throughout the enamel and share any physical burdens placed on a tooth, so that no one part has to take the full brunt.
By pressing down on individual teeth using a metal rod, Chai found that it’s relatively easy to create a crack in a tooth, but much harder to actually make it grow bigger to the point where the tooth properly breaks. The tufts, together with structures that prevent cracks from growing, are responsible – they allow us to chew without catastrophe. Our teeth aren’t built to avoid damage, but they’re incredibly good at containing it.
Humans aren’t alone in this – Chai compared out teeth to those of sea otters, and found the same adaptive features under a microscope. It may seem like an odd pairing, but we share a fondness for hard-shelled foods with sea otters – we like nuts and seeds, while they can’t get enough of shellfish. These similarities are reflected in our teeth.