Turing pattern

[3] Prior to the discovery of this instability mechanism arising due to unequal diffusion coefficients of the two substances, diffusional effects were always presumed to have stabilizing influences on the system.

Studies in chick and mouse embryonic development suggest that the patterns of feather and hair-follicle precursors can be formed without a morphogen pre-pattern, and instead are generated through self-aggregation of mesenchymal cells underlying the skin.

[17] It is a major theory in developmental biology; the importance of the Turing model is obvious, as it provides an answer to the fundamental question of morphogenesis: “how is spatial information generated in organisms?”.

A mechanism that has gained increasing attention as a generator of spot- and stripe-like patterns in developmental systems is related to the chemical reaction-diffusion process described by Turing in 1952.

Reaction-diffusion models can be used to forecast the exact location of the tooth cusps in mice and voles based on differences in gene expression patterns.

[8] The model can be used to explain the differences in gene expression between mice and vole teeth, the signaling center of the tooth, enamel knot, secrets BMPs, FGFs and Shh.

Under this model, the large differences between mouse and vole molars can be generated by small changes in the binding constants and diffusion rates of the BMP and Shh proteins.

A small increase in the diffusion rate of BMP4 and a stronger binding constant of its inhibitor is sufficient to change the vole pattern of tooth growth into that of the mouse.