Regulatory aspects of alkali tolerance induction in Escherichia coli

Escherichia coli shifted from external pH (pH(O)) 7.0 to pH(O) 8.5-9.5 rapidly becomes tolerant to pH(O) 10.0-11.5, induction of tolerance (alkali habituation) being dependent on periplasmic or external alkalinization with either NaOH or KOH. Induction needs protein synthesis and makes organisms resistant to DNA damage by alkali and better able to repair any damage that occurs. Induction of tolerance was reduced by glucose (not reversed by cAMP) and by amiloride, was dependent on DNA gyrase and was abolished by fur and himA lesions (the latter suggests IHF involvement). Tolerance induction was not prevented by L-leucine, FeCl3 or FeSO4 nor by hns or relA mutations. Habituation probably involves attachment of IHF upstream of the promoter leading to DNA bending which switches on transcription. Habituation is aberrant in nhaA mutants, so ability to resist alkali damage may only arise if NhaA is induced, with extrusion of Na+ by this antiporter during alkali challenge. In accord with one tolerance component involving NhaA induction, beta-galactosidase formation from nhaA-lacZ fusions at pH(O) 9.0 was inhibited by glucose and amiloride.