Robustness of Cellular Functions

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Robustness of Cellular Functions Jörg Stelling, Uwe Sauer, Zoltan Szallasi, Francis J. Doyle, John Doyle  Cell  Volume 118, Issue 6, Pages 675-685 (September 2004) DOI: 10.1016/j.cell.2004.09.008

Figure 1 Mapping from Parameter Space to Behavior Space Here, we calculated the relative period of oscillations for a simplified model of the circadian clock in Drosophila (Leloup and Goldbeter, 1998) depending on two of the model's parameters, namely, the maximal rates for transcription of per and tim. Gray lines indicate the reference point regarding the parameter values, at which oscillations have a period of approximately 24 hr. In the white region, no oscillations occur. Cell 2004 118, 675-685DOI: (10.1016/j.cell.2004.09.008)

Figure 2 Control by Negative Feedback (A) General scheme of negative feedback showing a plant (cellular function that is to be controlled) and a controller (regulatory circuit) that feeds back to the plant's input. We consider integral feedback control, where the output signal has to track a reference signal despite perturbations. (B) Rejection of a disturbance when the gain of the feedback loop is varied from low (black) to high (light gray). Cell 2004 118, 675-685DOI: (10.1016/j.cell.2004.09.008)

Figure 3 Logic of Chemotaxis Pathways in E. coli and B. subtilis Homologous Che proteins operate in both organisms (gray ellipses), but some components occur only in E. coli (green ellipses) or in B. subtilis (blue ellipses). Similarly, most of the interactions that control receptor modification by methylation and phosphorylation of the regulators are shared (black lines); colors indicate organism-specific detail. In response to an attractant, the overall regulation results in an increased running frequency, enabling the bacteria to move into the direction of a gradient. As denoted by the small circles, however, the signs of interactions have to differ because ligand binding reduces CheA activity in E. coli but increases it in B. subtilis. The figure was adapted from Rao et al. (2004), which provides additional detail on the regulatory mechanisms. Cell 2004 118, 675-685DOI: (10.1016/j.cell.2004.09.008)

Figure 4 Distribution of Metabolic Fluxes at the Glycolysis-Krebs Cycle Interface in E. coli Top entries in the boxes denote fluxes in wild-type, whereas bottom entries provide the values for a knockout mutant of both pyruvate and kinase isoenzymes. Flux values are relative to the specific glucose uptake rate and were obtained from glucose-limited continuous cultures at a growth rate of 0.4 h−1 (Emmerling et al., 2002). The local bypass of pyruvate kinase via malic enzyme and PEP carboxylase is highlighted with bold arrows. Cell 2004 118, 675-685DOI: (10.1016/j.cell.2004.09.008)