In 1952, well before developmental biologists spoke in terms of Hox genes and transcription factors, or even understood DNA’s structure, Alan Turing had an idea. The famed mathematician who hastened the end of World War II by cracking the Enigma code turned his mind to the natural world and devised an elegant mathematical model of pattern formation. His theory outlined how endless varieties of stripes, spots and scales could emerge from the interaction of two simple, hypothetical chemical agents, or “morphogens.”

Decades passed before biologists seriously considered that this mathematical theory could in fact explain myriad biological patterns. The development of mammalian hair, the feathers of birds and even those ridges on the roof of your mouth all stem from Turing-like mechanisms.

Now, denticles, the toothlike protrusions that cover the skin of sharks, can be added to the list. Researchers from the University of Florida recently discovered that shark denticles are laid down by a Turing-like mechanism directed by the same genes responsible for feather pattern formation. According to Gareth Fraser, the researcher who led the study, the work suggests that the developing embryos of diverse backboned species set down patterns of features in their outer layers of tissue in the same way — a patterning mechanism “that likely evolved with the first vertebrates and has changed very little since.”

“The beauty of this work is that it shows that there might be a very strong conservation of this mechanism for forming anything from shark denticles to bird feathers,” said Alexander Schier, a Harvard developmental biologist who was not involved in the study. This study bolsters a growing theme in developmental biology, that “nature tends to invent something once, and then plays variations on that theme,” Schier said.

Turing’s model, called a reaction-diffusion mechanism, is beautifully simple. It requires only two interacting agents, an activator and an inhibitor, that diffuse through tissue like ink dropped in water. The activator initiates some process, like the formation of a spot, and promotes the production of itself. The inhibitor halts both actions. Critically, the inhibitor spreads through tissue more quickly than the activator does. This faster diffusion of the inhibitor prevents pockets of activation from spilling over. Depending on exactly when and where the activator and inhibitor are released, the pockets of activation will arrange themselves as regularly spaced dots, stripes or other patterns.