REGULATORY ASPECTS OF ALKALI TOLERANCE INDUCTION IN ESCHERICHIA-COLI

Escherichia coli shifted from external pH (pH(0)) 7.0 to pH(0) 8.5-9.5 rapidly becomes tolerant to pH(0) 10.0-11.5, induction of tolerance ( alkali habituation) being dependent on periplasmic or external alkalin ization 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 g lucose (not reversed by cAMP) and by amiloride, was dependent on DNA g yrase and was abolished by fur and himA lesions (the latter suggests I I-IF involvement). Tolerance induction was not prevented by L-leucine, FeCl3 or FeSO4 nor by hns or relA mutations. Habituation probably inv olves attachment of IHF upstream of the promoter leading to DNA bendin g which switches on transcription. Habituation is aberrant in nhaA mut ants, so ability to resist alkali damage may only arise if NhaA is ind uced, with extrusion of Na+ by this antiporter during alkali challenge . In accord with one tolerance component involving NhaA induction, bet a-galactosidase formation from nhaA-lacZ fusions at pH(0) 9.0 was inhi bited by glucose and amiloride.