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Register a new userDynamics of glucose-lactose diauxic growth in E. coli
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We present a mathematical model of glucose-lactose diauxic growth in Escherichia coli including both the postive and negative regulation mechanisms of the lactose operon as well as the inducer exclusion. To validate this model, we first calculated the time evolution of beta-galactosidase for only the lactose nutrient and compared the numerical results with experimental data. Second, we compared the calculated cell biomass of the glucose-lactose diauxic growth with the experimental optical density of the diauxic growth for a particular E. coli MG 1655. For both cases, the numerical calculations from this model are in good agreement with these two experiments data. The diauxic growth pattern of a wild type E. coli was also investigated.
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Organisms must acquire and use environmental information to guide their behaviors. However, it is unclear whether and how information quantitatively limits behavioral performance. Here, we relate information to behavioral performance in Escherichia coli chemotaxis. First, we derive a theoretical limit for the maximum achievable gradient-climbing speed given a cells information acquisition rate. Next, we measure cells gradient-climbing speeds and the rate of information acquisition by the chemotaxis pathway. We find that E. coli make behavioral decisions with much less than the 1 bit required to determine whether they are swimming up-gradient. However, they use this information efficiently, performing near the theoretical limit. Thus, information can limit organisms performance, and sensory-motor pathways may have evolved to efficiently use information from the environment.
The mean size of exponentially dividing E. coli cells cultured in different nutrient conditions is known to depend on the mean growth rate only. However, the joint fluctuations relating cell size, doubling time and individual growth rate are only starting to be characterized. Recent studies in bacteria (i) revealed the near constancy of the size extension in a single cell cycle (adder mechanism), and (ii) reported a universal trend where the spread in both size and doubling times is a linear function of the population means of these variables. Here, we combine experiments and theory and use scaling concepts to elucidate the constraints posed by the second observation on the division control mechanism and on the joint fluctuations of sizes and doubling times. We found that scaling relations based on the means both collapse size and doubling-time distributions across different conditions, and explain how the shape of their joint fluctuations deviates from the means. Our data on these joint fluctuations highlight the importance of cell individuality: single cells do not follow the dependence observed for the means between size and either growth rate or inverse doubling time. Our calculations show that these results emerge from a broad class of division control mechanisms (including the adder mechanism as a particular case) requiring a certain scaling form of the so-called division hazard rate function, which defines the probability rate of dividing as a function of measurable parameters. This gives a rationale for the universal body-size distributions observed in microbial ecosystems across many microbial species, presumably dividing with multiple mechanisms. Additionally, our experiments show a crossover between fast and slow growth in the relation between individual-cell growth rate and division time, which can be understood in terms of different regimes of genome replication control.
Bacteria have remarkably robust cell shape control mechanisms. For example, cell diameter only varies by a few percent across a population. MreB is necessary for establishment and maintenance of rod shape although the mechanism of shape control remains unknown. We perturbed MreB in two complimentary ways to produce steady-state cell diameters over a wide range, from 790+/-30 nm to 1700+/-20 nm. To determine which properties of MreB are important for diameter control, we correlated structural characteristics of fluorescently-tagged MreB polymers with cell diameter by simultaneously analyzing 3-dimensional images of MreB and cell shape. Our results indicate that the pitch angle of MreB inversely correlates with cell diameter. Other correlations are not found to be significant. These results demonstrate that the physical properties of MreB filaments are important for shape control and support a model in which MreB dictates cell diameter and organizes cell wall growth to produce a chiral cell wall.
When analysing in vitro data, growth kinetics of influenza strains are often compared by computing their growth rates, which are sometimes used as proxies for fitness. However, analogous to mechanistic epidemic models, the growth rate can be defined as a function of two parameters: the basic reproduction number (the average number of cells each infected cell infects) and the mean generation time (the average length of a replication cycle). Using a mechanistic model, previously published data from experiments in human lung cells, and newly generated data, we compared estimates of all three parameters for six influenza A strains. Using previously published data, we found that the two human-adapted strains (pre-2009 seasonal H1N1, and pandemic H1N1) had a lower basic reproduction number, shorter mean generation time and slower growth rate than the two avian-adapted strains (H5N1 and H7N9). These same differences were then observed in data from new experiments where two strains were engineered to have different internal proteins (pandemic H1N1 and H5N1), but the same surface proteins (PR8), confirming our initial findings and implying that differences between strains were driven by internal genes. Also, the model predicted that the human-adapted strains underwent more replication cycles than the avian-adapted strains by the time of peak viral load, potentially accumulating mutations more quickly. These results suggest that the in vitro reproduction number, generation time and growth rate differ between human-adapted and avian-adapted influenza strains, and thus could be used to assess host adaptation of internal proteins to inform pandemic risk assessment.
Understanding the organization of reaction fluxes in cellular metabolism from the stoichiometry and the topology of the underlying biochemical network is a central issue in systems biology. In this task, it is important to devise reasonable approximation schemes that rely on the stoichiometric data only, because full-scale kinetic approaches are computationally affordable only for small networks (e.g. red blood cells, about 50 reactions). Methods commonly employed are based on finding the stationary flux configurations that satisfy mass-balance conditions for metabolites, often coupling them to local optimization rules (e.g. maximization of biomass production) to reduce the size of the solution space to a single point. Such methods have been widely applied and have proven able to reproduce experimental findings for relatively simple organisms in specific conditions. Here we define and study a constraint-based model of cellular metabolism where neither mass balance nor flux stationarity are postulated, and where the relevant flux configurations optimize the global growth of the system. In the case of E. coli, steady flux states are recovered as solutions, though mass-balance conditions are violated for some metabolites, implying a non-zero net production of the latter. Such solutions furthermore turn out to provide the correct statistics of fluxes for the bacterium E. coli in different environments and compare well with the available experimental evidence on individual fluxes. Conserved metabolic pools play a key role in determining growth rate and flux variability. Finally, we are able to connect phenomenological gene essentiality with `frozen fluxes (i.e. fluxes with smaller allowed variability) in E. coli metabolism.
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