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Review
. 2009 Dec;12(6):667-73.
doi: 10.1016/j.mib.2009.09.006. Epub 2009 Oct 23.

Signals of growth regulation in bacteria

Christopher S Hayes  1 , David A Low
Affiliations
Review

Signals of growth regulation in bacteria

Christopher S Hayes et al. Curr Opin Microbiol. 2009 Dec.

Abstract

A fundamental characteristic of cells is their ability to regulate growth in response to changing environmental conditions. This review focuses on recent progress toward understanding the mechanisms by which bacterial growth is regulated. These phenomena include the 'viable but not culturable' (VBNC) state, in which bacterial growth becomes conditional, and 'persistence', which confers antibiotic resistance to a small fraction of bacteria in a population. Notably, at least one form of persistence appears to involve the generation of nongrowing phenotypic variants after transition through stationary phase. The possible roles of toxin-antitoxin modules in growth control are explored, as well as other mechanisms including contact-dependent growth inhibition, which regulates cellular metabolism and growth through binding to an outer membrane protein receptor.

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Figures

Figure. 1
Figure. 1. Examples of contact-dependent alteration in metabolism and growth
(A). Escherichia coli containing the cdiBAI genes express CdiB, which is predicted to reside in the outer membrane and function in export of CdiA to the cell surface. CdiA is postulated to mediate binding to the BamA receptor in the outer membrane (OM) of target cells, and reduce the proton gradient, respiration, ATP, and cell growth/division of target cells. CdiI provides immunity to autoinhibition by cognate CdiA effector. The CDI mechanism may involve interaction with the multidrug efflux pump AcrB located in the inner membrane (IM) [6,7,9] . (B). Pelotomaculum thermopropionicum strain S1 expresses flagella that bind to its syntrophic partner Methanothermobacter thermoautotrophicus strain △H, keeping the cells close by tethering. Binding of the FliD cap protein of the flagellum to an unidentified receptor on M. thermoautotrophicus alters cellular metabolism including induction of methane formation. Hydrogen gas from P. thermopropionicum is used for methane production, and serving to keep H2 levels low and enabling continued fermentation of propionate by P. thermopropionicum •[12].
Figure 2
Figure 2. Toxin-antitoxin (TA) module organization and the stress-response regulator hypothesis
(A) TA module genetic organization. TA systems are typically two-gene operons with the antitoxin encoded upstream of the toxin gene. Proteic antitoxins bind their cognate toxins and inhibit toxin activity. Antitoxins and toxin-antitoxin complexes repress TA module transcription. In Escherichia coli, toxin activation involves degradation of antitoxin by either the Lon or ClpAP proteases. Activated toxins inhibit cell growth and/or lead to cell death. (B) The stress-response regulator hypothesis of chromosomal TA function. Environmental stresses such as starvation activate chromosomal TA modules through antitoxin degradation. Many toxins are mRNA-specific RNases that rapidly inhibit protein synthesis, inducing a bacteriostatic state. Upon adaptation (or removal of the stress), antitoxin synthesis resumes to counteract toxin activity, and tmRNA activity rescues ribosomes arrested on toxin-cleaved messages.
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