The evolution of robust development and homeostasis in artificial organisms.
During embryogenesis, multicellular animals are shaped via cell proliferation, cell rearrangement, and apoptosis. At the end of development, tissue architecture is then maintained through balanced rates of cell proliferation and loss. Here, we take an in silico approach to look for generic systems features of morphogenesis in multicellular animals that arise as a consequence of the evolution of development. Using artificial evolution, we evolved cellular automata-based digital organisms that have distinct embryonic and homeostatic phases of development. Although these evolved organisms use a variety of strategies to maintain their form over time, organisms of different types were all found to rapidly recover from environmental damage in the form of wounds. This regenerative response was most robust in an organism with a stratified tissue-like architecture. An evolutionary analysis revealed that evolution itself contributed to the ability of this organism to maintain its form in the face of genetic and environmental perturbation, confirming the results of previous studies. In addition, the exceptional robustness of this organism to surface injury was found to result from an upward flux of cells, driven in part by cell divisions with a stable niche at the tissue base. Given the general nature of the model, our results lead us to suggest that many of the robust systems properties observed in real organisms, including scar-free wound-healing in well-protected embryos and the layered tissue architecture of regenerating epithelial tissues, may be by-products of the evolution of morphogenesis, rather than the direct result of selection.
Basanta
David
D
Materials Research Group, Engineering Division, King's College London, London, United Kingdom.
Miodownik
Mark
M
Baum
Buzz
B
D000818:Animals; D005075:Biological Evolution; D032701:Biomimetics / Q000379:methods*; D002450:Cell Communication / Q000502:physiology*; D002468:Cell Physiological Phenomena; D003198:Computer Simulation; D006706:Homeostasis / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009024:Morphogenesis / Q000502:physiology*; D012038:Regeneration / Q000502:physiology*