MMBR Figure table search 04
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Marr, A G
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marr, A G

 Previous Article  |  Next Article 

Microbiol Mol Biol Rev. 1991 June; 55(2): 316-333

Growth rate of Escherichia coli.

A G Marr

Department of Microbiology, University of California, Davis 95616.

SUMMARY

It should be possible to predict the rate of growth of Escherichia coli of a given genotype in a specified environment. The idea that the rate of synthesis of ATP determines the rate of growth and that the yield of ATP determines the yield of growth is entrenched in bacterial physiology, yet this idea is inconsistent with experimental results. In minimal media the growth rate and yield vary with the carbon source in a manner independent of the rate of formation and yield of ATP. With acetate as the carbon source, anapleurotic reactions, not ATP synthesis, limit the growth rate. For acetate and other gluconeogenic substrates the limiting step appears to be the formation of triose phosphate. I conclude that the rate of growth is controlled by the rate of formation of a precursor metabolite and, thus, of monomers such as amino acids derived from it. The protein-synthesizing system is regulated according to demand for protein synthesis. I examine the conjecture that the signal for this regulation is the ratio of uncharged tRNA to aminoacyl-tRNA, that this signal controls the concentration of guanosine tetraphosphate, and that the concentration of guanosine tetraphosphate controls transcription of rrn genes. Differential equations describing this system were solved numerically for steady states of growth; the computed values of ribosomes and guanosine tetraphosphate and the maximal growth rate agree with experimental values obtained from the literature of the past 35 years. These equations were also solved for dynamical states corresponding to nutritional shifts up and down.


Microbiol Mol Biol Rev. 1991 June; 55(2): 316-333




This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. J. Bacteriol.
ALL ASM JOURNALS

Copyright © 1991 by the American Society for Microbiology. All rights reserved.