 | Complexity in Regulation Generates Robustness in Bacterial Molecular Networks
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| | Hiroyuki Kurata1)2) and Kazunari Taira1)3) |
| 1) Department of Chemistry and Biotechnology The University of Tokyo
2) Research Advisor, Systems Biology Group, ERATO Kitano Symbiotic Systems Project, JST
3) National Institute for Advanced Interdisciplinary Research, AIST, MITI Tsukuba Science City |
| | There is a question of how one can understand a biological system composed of heterogeneous and interactive subsystems. If the interaction among subsystems is sensitive, one cannot analyze smaller subsystems separately. If their interaction shows robustness, one can extract a subsystem out of the whole system, analyzing them one by one. In the heat shock response, σ32 (encoded the rpoH gene) plays a major role in controlling expression of heat shock protein genes that encode chaperones and proteases. The level of active σ32 is regulated by complex mechanisms: chaperone-mediated regulation of σ32 activity and stability, thermoregulated-induction of the rpoH mRNA, and protease-mediated degradation of σ32. The numerical framework model shows that complexity in σ32 regulation generates robustness in the E. coli heat shock response, thereby increasing the robustness of the interconnected factors among subsystems. Complexity seems to impede isolating a smaller subsystem out of a whole biological system. Actually, complexity generates robustness among subsystems, thereby making it possible to extract a smaller subsystem out of the whole system and analyze it separately. |
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