The detailed mechanism of Turing pattern formation in the skin of zebrafish

S Kondo

Graduate School of Frontier BioScience, Osaka University, 565-0871, Suita, Osaka, Japan

The reaction-diffusion (RD) model presented by Alan Turing in 1952 is a theoretical mechanism to explain how spatial patterns form autonomously in an organism. In his classic paper, Turing examined the behaviour of a system in which two diffusible substances interact with each other, and found that such a system is able to generate a spatially periodic pattern even from a random or almost uniform initial condition. Turing hypothesized that the resulting wavelike patterns are the chemical basis of morphogenesis. The importance of the Turing model is obvious, in that it provided an answer to the fundamental question of morphogenesis: "how is spatial information generated in organisms?" However, most experimental researchers were sceptical until the mid-90s because little convincing evidence had been presented. In 1991, two groups of physicists succeeded in generating the Turing patterns in their artificial systems, which showed for the first time that the Turing wave is not a fantasy but a reality in science. Four years later, we reported that the stripes of colour on the skin of some tropical fishes are dynamically rearranged during development in accordance with Turing model predictions. Soon after, convincing experimental evidence claiming the involvement of a Turing mechanism in development has been reported, and in some cases, the candidate diffusible molecules were suggested. Currently, the Turing model has been accepted as one of the fundamental mechanisms that govern morphogenesis. On the other hand, experimental researchers have pointed out problem that occur when the Turing model or other derivative models (called as LALI models because Local Activation and Long range Inhibition is required) are used as the working hypothesis. For instance, LALI models can exhibit similar properties of pattern formation despite being based on different cellular and molecular functions. Therefore, the simulation of a model rarely helps to identify the detailed molecular mechanism. Even when a pattern-forming phenomenon is successfully reproduced by the simulation of an RD system, it does not guarantee the involvement of diffusion. This problem is quite serious because, in most experimental uses, the key molecular event that governs the phenomenon is unknown when the experimental project begins. In my talk, I will explain the experimental data proving that Turing-like mechanism really functions in the skin of zebrafish, and then, I will propose a new version of the Turing model that might compliment the shortcomings of the present model.