SENSITIZATION TO ACID-INDUCED BY SODIUM-IONS IN ESCHERICHIA-COLI - DEPENDENCE ON (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 pressu re but is triggered by a high internal sodium ion concentration, evide nced by the finding that conditions which enhance Na+ influx or reduce Na+ efflux, led to increased internal Na+ and allowed induction at lo wer external sodium ion concentrations and that induction could occur with no osmotic upshock. NaCl-induced acid sensitivity was not observe d in Escherichia coli strain MC4100 and its relA lesion was investigat ed as a possible cause. Transformation of this strain and two other re lA 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 d erivatives 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 o f sensitization was slightly increased by fur and considerably increas ed by tonB. Acetate strongly inhibited sensitization, which was also s ubject 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 wit h this, high concentrations of cAMP suppressed the effect of the relA lesion on sensitization. Salt-induced organisms are more sensitive to acid damage to DNA, to acid inhibition of enzyme synthesis and DNA tra nsfer and slightly less able to repair acid-damaged transforming DNA.