TY - JOUR
T1 - rpoS mutations and loss of general stress resistance in Escherichia coli populations as a consequence of conflict between competing stress responses
AU - Notley-McRobb, Lucinda
AU - King, Thea
AU - Ferenci, Thomas
PY - 2002
Y1 - 2002
N2 - The general stress resistance of Escherichia coli is controlled by the RpoS sigma factor (σs), 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 σs levels. Competition for core RNA polymerase is the likeliest explanation for reduced expression from distinct promoters dependent on σ70 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 σs 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.
AB - The general stress resistance of Escherichia coli is controlled by the RpoS sigma factor (σs), 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 σs levels. Competition for core RNA polymerase is the likeliest explanation for reduced expression from distinct promoters dependent on σ70 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 σs 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.
UR - http://www.scopus.com/inward/record.url?scp=0036181664&partnerID=8YFLogxK
M3 - Article
C2 - 11790751
AN - SCOPUS:0036181664
VL - 184
SP - 806
EP - 811
JO - Journal of Bacteriology
JF - Journal of Bacteriology
SN - 0021-9193
IS - 3
ER -