rpoS mutations and loss of general stress resistance in Escherichia coli populations as a consequence of conflict between competing stress responses.
The general stress resistance of Escherichia coli is controlled by the RpoS sigma factor (phi(S)), but mutations in rpoS are surprisingly common in natural and laboratory populations. Evidence for the selective advantage of losing rpoS was obtained from experiments with nutrient-limited bacteria at different growth rates. Wild-type bacteria were rapidly displaced by rpoS mutants in both glucose- and nitrogen-limited chemostat populations. Nutrient limitation led to selection and sweeps of rpoS null mutations and loss of general stress resistance. The rate of takeover by rpoS mutants was most rapid (within 10 generations of culture) in slower-growing populations that initially express higher phi(S) levels. Competition for core RNA polymerase is the likeliest explanation for reduced expression from distinct promoters dependent on phi(70) and involved in the hunger response to nutrient limitation. Indeed, the mutation of rpoS led to significantly higher expression of genes contributing to the high-affinity glucose scavenging system required for the hunger response. Hence, rpoS polymorphism in E. coli populations may be viewed as the result of competition between the hunger response, which requires sigma factors other than phi(S) for expression, and the maintenance of the ability to withstand external stresses. The extent of external stress significantly influences the spread of rpoS mutations. When acid stress was simultaneously applied to glucose-limited cultures, both the phenotype and frequency of rpoS mutations were attenuated in line with the level of stress. The conflict between the hunger response and maintenance of stress resistance is a potential weakness in bacterial regulation.
Notley-McRobb
Lucinda
L
Department of Microbiology, University of Sydney, Sydney, New South Wales 2006, Australia.
King
Thea
T
Ferenci
Thomas
T
D001426:Bacterial Proteins / Q000235:genetics*; D001693:Biological Transport, Active; D004926:Escherichia coli / Q000502:physiology*; D015964:Gene Expression Regulation, Bacterial; D005947:Glucose / Q000172:deficiency* / Q000378:metabolism; D009154:Mutation; D009584:Nitrogen / Q000172:deficiency* / Q000378:metabolism; D012808:Sigma Factor / Q000235:genetics*
D001426:Bacterial Proteins; D012808:Sigma Factor; C069567:sigma factor KatF protein, Bacteria; D005947:Glucose; D009584:Nitrogen