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Non‐growing Escherichia coli cells starved for glucose or phosphate use different mechanisms to survive oxidative stress ‡
Author(s) -
Moreau Patrice L.,
Gérard Fabien,
Lutz Norbert W.,
Cozzone Patrick
Publication year - 2001
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2001.02303.x
Subject(s) - biology , escherichia coli , rpos , biochemistry , superoxide dismutase , oxidative stress , viability assay , gene , cell , gene expression , promoter
Recent data suggest that superoxide dismutases are important in preventing lethal oxidative damage of proteins in Escherichia coli cells incubated under aerobic, carbon starvation conditions. Here, we show that the alkylhydroperoxide reductase AhpCF (AHP) is specifically required to protect cells incubated under aerobic, phosphate (Pi) starvation conditions. Additional loss of the HP‐I (KatG) hydroperoxidase activity dramatically accelerated the death rate of AHP‐deficient cells. Investigation of the composition of spent culture media indicates that Δ ahpCF katG cells leak nutrients, which suggests that membrane lipids are the principal target of peroxides produced in Pi‐starved cells. In fact, the introduction of various mutations inactivating repair activities revealed no obvious role for protein or DNA lesions in the viability of ahp cells. Because the death of ahp cells was directly related to ongoing aerobic glucose metabolism, we wondered how glycolysis, which requires free Pi, could proceed. 31 P nuclear magnetic resonance spectra showed that Pi‐starved cells consumed Pi but were apparently able to liberate Pi from phosphorylated products, notably through the synthesis of UDP‐glucose. Whereas expression of the ahpCF and katG genes is enhanced in an OxyR‐dependent manner in response to H 2 O 2 challenge, we found that the inactivation of oxyR and both oxyR and rpoS genes had little effect on the viability of Pi‐starved cells. In stark contrast, the inactivation of both oxyR and rpoS genes dramatically decreased the viability of glucose‐starved cells.