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Contact-dependent growth inhibition causes reversible metabolic downregulation in Escherichia coli

Contact-dependent growth inhibition causes reversible metabolic downregulation in Escherichia coli
Contact-dependent growth inhibition causes reversible metabolic downregulation in Escherichia coli
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 (Deltap), and steady-state ATP levels. It is unclear whether the decrease in respiration and/or Deltap 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 Deltap, the phage shock response was induced in cells undergoing CDI but not in recovering cells, based on analysis of levels of pspA mRNA.
0021-9193
1777-1786
Aoki, S. K.
61e8ecc9-b64f-4abb-8e7a-5bc583250741
Webb, Jeremy
ec0a5c4e-86cc-4ae9-b390-7298f5d65f8d
Braaten, B. A.
a6e38362-2186-4494-a34f-718372ade757
Low, D. A.
255b06ad-ac5b-48e3-bed1-67a9e64e9ad6
Aoki, S. K.
61e8ecc9-b64f-4abb-8e7a-5bc583250741
Webb, Jeremy
ec0a5c4e-86cc-4ae9-b390-7298f5d65f8d
Braaten, B. A.
a6e38362-2186-4494-a34f-718372ade757
Low, D. A.
255b06ad-ac5b-48e3-bed1-67a9e64e9ad6

Aoki, S. K., Webb, Jeremy, Braaten, B. A. and Low, D. A. (2009) Contact-dependent growth inhibition causes reversible metabolic downregulation in Escherichia coli. Journal of Bacteriology, 191 (6), 1777-1786. (doi:10.1128/JB.01437-08).

Record type: Article

Abstract

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 (Deltap), and steady-state ATP levels. It is unclear whether the decrease in respiration and/or Deltap 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 Deltap, the phage shock response was induced in cells undergoing CDI but not in recovering cells, based on analysis of levels of pspA mRNA.

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Accepted/In Press date: 23 December 2008
Published date: 1 March 2009

Identifiers

Local EPrints ID: 442646
URI: http://eprints.soton.ac.uk/id/eprint/442646
ISSN: 0021-9193
PURE UUID: 0bd4c356-9f0a-4a54-a50b-48d7b689c833
ORCID for Jeremy Webb: ORCID iD orcid.org/0000-0003-2068-8589

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Date deposited: 22 Jul 2020 16:31
Last modified: 18 Feb 2021 17:08

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Contributors

Author: S. K. Aoki
Author: Jeremy Webb ORCID iD
Author: B. A. Braaten
Author: D. A. Low

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