Sensitization to acid induced by sodium ions in Escherichia coli: dependence of (p)ppGpp and cAMP and suppression of the relA-associated defect by mutations in envZ.
NaCl-induced acid sensitivity is not a response to high osmotic pressure but is triggered by a high internal sodium ion concentration, evidenced by the finding that conditions which enhance Na+ influx or reduce Na+ efflux, led to increased internal Na+ and allowed induction at lower external sodium ion concentrations and that induction could occur with no osmotic upshock. NaCl-induced acid sensitivity was not observed in Escherichia coli strain MC4100 and its relA lesion was investigated as a possible cause. Transformation of this strain and two other relA mutants to relA+ allowed sensitization by NaCl and whereas strain CF1648 (relA+) was sensitized, its relA deletion derivative was not. Additionally, transduction of two relA+ strains to relA produced derivatives which were not sensitized by salt. Although MC4100 was not sensitized by NaCl, envZ derivatives of it were sensitized. Lesions in fur and tonB did not prevent sensitization by NaCl, although extent of sensitization was slightly increased by fur and considerably increased by tonB. Acetate strongly inhibited sensitization, which was also subject to glucose repression, reversible by cAMP. The possibility was discussed that (p)ppGpp and cAMP both positively affect transcription of the genes encoding the acid sensitization components; in accord with this, high concentrations of cAMP suppressed the effect of the relA lesion of sensitization. Salt-induced organisms are more sensitive to acid damage to DNA, to acid inhibition of enzyme synthesis and DNA transfer and slightly less able to repair acid-damaged transforming DNA.
Rowbury
R J
RJ
Biology Department (Darwin), University College London, Great Britain.
Goodson
M
M
Lazim
Z
Z
Humphrey
T J
TJ
D001425:Bacterial Outer Membrane Proteins / Q000235:genetics / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism*; D004917:Erythromycin / Q000494:pharmacology; D004926:Escherichia coli / Q000187:drug effects / Q000378:metabolism*; D029968:Escherichia coli Proteins; D006159:Guanosine Tetraphosphate / Q000378:metabolism*; D006851:Hydrochloric Acid / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D008025:Ligases / Q000235:genetics / Q000378:metabolism*; D009097:Multienzyme Complexes; D012293:Rifampin / Q000494:pharmacology; D012965:Sodium Chloride / Q000494:pharmacology*; D013489:Suppression, Genetic; D014640:Vancomycin / Q000494:pharmacology
D001425:Bacterial Outer Membrane Proteins; D029968:Escherichia coli Proteins; D009097:Multienzyme Complexes; D006159:Guanosine Tetraphosphate; D012965:Sodium Chloride; D004917:Erythromycin; D014640:Vancomycin; D000242:Cyclic AMP; C057843:envZ protein, E coli; D008025:Ligases; C028812:guanosine 3',5'-polyphosphate synthetases; D006851:Hydrochloric Acid; D012293:Rifampin