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Mutations in two global regulators lower individual mortality in Escherichia coli
Fanette Fontaine, 1,2,3 Eric J. Stewart, 1,3 Ariel B. Lindner 1,3 and François Taddei 1,3 *
  1 Inserm, U571, Paris, F-75015, France.
  2 Université Pierre et Marie Curie, Paris, F-75005, France.
  3 Université Paris Descartes, Fac Med Necker, Paris, F-75730, France.
Correspondence to   *E-mail taddei@necker.fr; Tel. (+33) 1 40 61 53 23; Fax (+33) 1 40 61 53 22.

   Present address: Northeastern University, Department of Biology, Boston, MA, USA.

 Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.

Copyright © 2007 The Authors; Journal compilation © 2007 Blackwell Publishing Ltd

ABSTRACT

There has been considerable investigation into the survival of bacterial cells under stress conditions, but little is known about the causes of mortality in the absence of exogenous stress. That there is a basal frequency of cell death in such populations may reflect that it is either impossible to avoid all lethal events, or alternatively, that it is too costly. Here, through a genetic screen in the model organism Escherichia coli, we identify two mutants with lower frequencies of mortality: rssB and fliA. Intriguingly, these two genes both affect the levels of different sigma factors within the cell. The rssB mutant displays enhanced resistance to multiple external stresses, possibly indicating that the cell gains its increased vitality through elevated resistance to spontaneous, endogenous stresses. The loss of fliA does not result in elevated stress resistance; rather, its survival is apparently due to a decreased physical stress linked to the insertion of the flagellum through the membrane and energy saved through the loss of the motor proteins. The identification of these two mutants implies that reducing mortality is not impossible; rather, due to its cost, it is subject to trade-offs with other traits that contribute to the competitive success of the organism.


Accepted 25 September, 2007.

DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1365-2958.2007.05988.x About DOI

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