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Journal of Bacteriology, March 2009, p. 1777-1786, Vol. 191, No. 6
0021-9193/09/$08.00+0     doi:10.1128/JB.01437-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Contact-Dependent Growth Inhibition Causes Reversible Metabolic Downregulation in Escherichia coli{triangledown}

S. K. Aoki, J. S. Webb, B. A. Braaten, and D. A. Low*

Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, California 93106

Received 13 October 2008/ Accepted 23 December 2008

Contact-dependent growth inhibition (CDI) is a mechanism identified in Escherichia coli by which bacteria expressing two-partner secretion proteins encoded by cdiA and cdiB bind to BamA in the outer membranes of target cells and inhibit their growth. A third gene in the cluster, cdiI, encodes a small protein that is necessary and sufficient to confer immunity to CDI, thereby preventing cells expressing the cdiBA genes from inhibiting their own growth. In this study, the cdiI gene was placed under araBAD promoter control to modulate levels of the immunity protein and thereby induce CDI by removal of arabinose. This CDI autoinhibition system was used for metabolic analyses of a single population of E. coli cells undergoing CDI. Contact-inhibited cells showed altered cell morphology, including the presence of filaments. Notably, CDI was reversible, as evidenced by resumption of cell growth and normal cellular morphology following induction of the CdiI immunity protein. Recovery of cells from CDI also required an energy source. Cells undergoing CDI showed a significant, reversible downregulation of metabolic parameters, including aerobic respiration, proton motive force ({Delta}p), and steady-state ATP levels. It is unclear whether the decrease in respiration and/or {Delta}p is directly involved in growth inhibition, but a role for ATP in the CDI mechanism was ruled out using an atp mutant. Consistent with the observed decrease in {Delta}p, the phage shock response was induced in cells undergoing CDI but not in recovering cells, based on analysis of levels of pspA mRNA.

* Corresponding author. Mailing address: Room 3129, Biosciences 2 Building, Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA 93106. Phone: (805) 893-5597. Fax: (805) 893-4724. E-mail: low{at}lifesci.ucsb.edu

{triangledown} Published ahead of print on 5 January 2009.

Journal of Bacteriology, March 2009, p. 1777-1786, Vol. 191, No. 6
0021-9193/09/$08.00+0     doi:10.1128/JB.01437-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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