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Testing Turing's theory of morphogenesis in chemical cells.

ABSTRACT: Alan Turing, in "The Chemical Basis of Morphogenesis" [Turing AM (1952) Philos Trans R Soc Lond 237(641):37-72], described how, in circular arrays of identical biological cells, diffusion can interact with chemical reactions to generate up to six periodic spatiotemporal chemical structures. Turing proposed that one of these structures, a stationary pattern with a chemically determined wavelength, is responsible for differentiation. We quantitatively test Turing's ideas in a cellular chemical system consisting of an emulsion of aqueous droplets containing the Belousov-Zhabotinsky oscillatory chemical reactants, dispersed in oil, and demonstrate that reaction-diffusion processes lead to chemical differentiation, which drives physical morphogenesis in chemical cells. We observe five of the six structures predicted by Turing. In 2D hexagonal arrays, a seventh structure emerges, incompatible with Turing's original model, which we explain by modifying the theory to include heterogeneity.

SUBMITTER: Tompkins N

PROVIDER: S-EPMC3970514 | biostudies-literature | 2014 Mar

REPOSITORIES: biostudies-literature

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Testing Turing's theory of morphogenesis in chemical cells.

Tompkins Nathan N Li Ning N Girabawe Camille C Heymann Michael M Ermentrout G Bard GB Epstein Irving R IR Fraden Seth S

Proceedings of the National Academy of Sciences of the United States of America 20140310 12

Alan Turing, in "The Chemical Basis of Morphogenesis" [Turing AM (1952) Philos Trans R Soc Lond 237(641):37-72], described how, in circular arrays of identical biological cells, diffusion can interact with chemical reactions to generate up to six periodic spatiotemporal chemical structures. Turing proposed that one of these structures, a stationary pattern with a chemically determined wavelength, is responsible for differentiation. We quantitatively test Turing's ideas in a cellular chemical sys ...[more]

PMID: 24616508

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Project description:Background: Information on the carcinogenic potential of chemicals is only availably for High Production Volume products. There is however, a pressing need for alternative methods allowing for the chronic toxicity of substances, including carcinogenicity, to be detected earlier and more reliably. Here we applied advanced genomics to a cellular transformation assay to identify gene signatures useful for the prediction of risk for carcinogenicity. Methods: Genome wide gene expression analysis and qRT-PCR were applied to untransformed and transformed Balb/c 3T3 cells that exposed to 2, 4-diaminotoluene (DAT), benzo(a)pyrene (BaP), 2-Acetylaminoflourene (AAF) and 3-methycholanthrene (MCA) for 24h and 120h, at different concentrations, respectively. Furthermore, various bioinformatics tools were used to identify gene signatures predicting for the carcinogenic risk. Results: Bioinformatics analysis revealed distinct datasets for the individual chemicals tested while the number of significantly regulated genes increased with ascending treatment concentration of the cell cultures. Filtering of the data revealed a common gene signature that comprised of 13 genes whose regulation in cancer tissue has already been established. Strikingly, this gene signature was already identified prior to cell transformation therefore confirming the predictive power of this gene signature in identifying carcinogenic risks of chemicals. Comparison of fold changes determined by microarray analysis and qRT-PCR were in good agreement. Conclusion: Our data describes selective and commonly regulated carcinogenic pathways observed in an easy to use in vitro carcinogenicity assay. Here we defined a set of genes which can serve as a simply assay to predict the risk for carcinogenicity by use of an alternative in vitro testing strategy. Balb/c 3T3 cells were seeded at 200 cells in each 60 x 15 mm culture dish with 4 ml M10F, using six culture dishes for every treatment. When cells reached a confluence of 60-65%, the culture medium was removed and replaced with fresh medium containing all tested chemicals at a specific concentration and two time points (24 and 120h). First we treated the cells both 24h and 120h with concentrations reported in the literature (0.5ÂµM BaP, 50ÂµM DAT, 25ÂµM AAF and 2ÂµM MCA). In a second approach IC20 concentrations were investigated for each chemical at both time points. The concentrations determined for IC20 ranged from 1.5 ÂµM BaP to 700 ÂµM DAT for 24h of treatment, and from 0.1 ÂµM BaP or MCA to 10ÂµM AAF for 120h of treatment. Balb/c 3T3 cells treated with 0.75% DMSO alone were kept as controls. Each experiment was run in triplicate.

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Testing Turing's theory of morphogenesis in chemical cells.

Publications

Testing Turing's theory of morphogenesis in chemical cells.

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