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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.
Highlights
Understanding the mechanisms underlying the survival of bacterial cells, defined as the capacity of the cell to Accepted 25 September, 2007. *For correspondence
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
Through a genetic screen in the model organism Escherichia coli, we identify two mutants with lower frequencies of mortality: rssB and fliA. These two genes both affect the levels of different sigma factors within the cell
Summary
Understanding the mechanisms underlying the survival of bacterial cells, defined as the capacity of the cell to Accepted 25 September, 2007. *For correspondence. Survival and death of the model organism Escherichia coli have been extensively studied on cells exposed to external sources of stress, such as high temperature, pH, UV, oxidative agents, antibiotics, high salt concentration, heavy metals and starvation (Storz and Hengge-Aronis, 1999; and references therein). Those studies have increased the understanding of how these external stresses injure cells and lead to the identification of several stress-response systems involved in the survival of bacterial cells. The nature of these pathways varies from very specific, such as the case of heavy metal resistance, where only a few genes are involved, to very general, such as the RpoS stress-response system, where more than 80 genes are co-ordinately regulated in response to a variety of stresses (Weber et al, 2005)
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