SODIUM-CHLORIDE INDUCES AN NHAA NHAR-INDEPENDENT ACID SENSITIVITY AT NEUTRAL EXTERNAL PH IN ESCHERICHIA-COLI

Escherichia coli previously grown in low-salt broth, pH 7.0, produced organisms which were markedly more acid sensitive when subsequently cu ltured in the same broth with 200 mM or more salt (NaCl) added. Induct ion of acid sensitivity occurred rapidly at both 37 and 30 degrees C, with a substantial effect within 15 min. Sensitization was partially i nhibited by chloramphenicol and tetracycline and may depend on both pr otein synthesis-dependent and -independent physiological changes in th e NaCl-induced organisms; sensitization did not result from osmotic sh ocking on transfer to challenge medium. Induction of acid sensitivity was affected by neither the sodium ion pore inhibitor amiloride nor th e DNA synthesis inhibitor nalidixic acid; rifampin had a small effect, similar to that of chloramphenicol. Chlorides of other monovalent cat ions, especially Li+ and NH4+, also produced sensitization to acid, al though CsCl was ineffective but did not interfere with sensitization b y NaCl. Other sodium salts were also active as sensitizers, as were ch lorides of divalent cations, but although sucrose (but not glycerol) w as a good inducer, the results were not fully in accord with triggerin g of induction solely by the NaCl-associated increase in osmotic press ure. Sensitization was not prevented by deletion of the nhaA, nhaR, or nhaB gene. Acid sensitivity of NaCl-induccd cells was slightly reduce d after 90 min of growth at 37 degrees C in low-salt broth but was com pletely lost after 240 min. For NaCl-induced cells, acid killing in ch allenge media was not inhibited by amiloride. The NaCl-induced sensiti zation is distinct from the phenomenon of acid sensitivity induction i n E. coli at alkaline external pH.