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GPCR‐controlled chemotaxis in Dictyostelium discoideum

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Abstract Dictyostelium discoideum has been chosen as the key model organism for the study of eukaryotic chemotaxis. Studies in this lower eukaryotic organism have allowed us to discover eukaryotic chemotaxis behavior and to gradually understand the mechanism of chemotaxis. Investigations in this simple organism often guide the direction of chemotaxis studies in areas such as forming concepts, discovering molecular components, revealing pathways and networks. The cooperation between experimental approaches and computational modeling has helped us to comprehend the signaling network as a system. To further reveal the relationships among the molecular mechanisms of individual signaling steps, a continuous interplay between model development and refinement and experimental testing and verification will be useful. This article focuses on a chemoattractant G‐protein‐coupled receptor (GPCR)/G‐protein gradient sensing machinery, which is monitored by PIP3 responses and investigated by the interplay between live cell imaging experiments and computational modeling. We believe that such an approach will lead to a much better understanding of GPCR‐controlled chemotaxis of all eukaryotic cells. WIREs Syst Biol Med 2011 3 717–727 DOI: 10.1002/wsbm.143 This article is a U.S. Government work, and as such, is in the public domain in the United States of America. This article is categorized under: Physiology > Physiology of Model Organisms

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Chemotaxis. (a) A simple model describes chemotaxis as a system. (b) Chemotaxis behavior of a bacterium. A gradient is shown as a shade of red color. (c) Chemotaxis behavior of eukaryotic amoeba. A leading front is shown as green regions.

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The interplay of determining dynamics of cAMP signaling network by live cell imaging, constructing signaling networking by SIMMUNE, and simulating dynamics in response to various cAMP stimulations.

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Modeling and computing kinetics of G‐protein dissociation in response to a saturating dose of cAMP. (a) A precoupling model induces a transient G‐protein dissociation because ligand‐bound receptor does not interact with heterotrimeric G‐proteins. (b) A ligand‐induced coupling model induces a persistent G‐protein dissociation. (c) Simulated kinetics of G‐protein dissociation upon a saturating dose of cAMP. (d) Simulated kinetics of G‐protein dissociation upon a saturating dose of cAMP.

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(a) A simple model explains adaptation process. (b) A model of signal network describes cAMP‐induced adaptation and gradient sensing. P1 shows a pathway that regulates PTEN activity. P2 is a pathway that inhibits signaling from Gβγ‐Ras‐PI3K.

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