PMID:8987702
| Citation |
Lazim, Z, Humphrey, TJ and Rowbury, RJ (1996) Induction of the PhoE porin by NaCl as the basis for salt-induced acid sensitivity in Escherichia coli. Lett. Appl. Microbiol. 23:269-72 |
|---|---|
| Abstract |
Organisms grown in low salt broth (LSB) are acid resistant but become sensitive on growth for 30-60 min with 300 mmol l-1 added NaCl. Salt-induced acid sensitivity only occurs in relA+ strains and sensitization is abolished by glucose, this catabolite repression effect being reversed by cAMP. The finding that sensitization did not occur in a phoE strain but did occur in a phoE+ derivative of it suggested that the response might result from PhoE induction, since PhoE acts as the major outer membrane (OM) proton pore under most conditions. In agreement with this, low-salt broth (LSB)-grown cells of a chromosomally lac- strain carrying pJP102 (phoE-lacZ) produced low levels of beta-galactosidase but growth with added NaCl led to rapid and appreciable induction. Also, a phoA mutant carrying a phoE-phoA fusion produced little alkaline phosphatase after growth in LSB but much more in LSB with added NaCl. Increased beta-galactosidase synthesis (in phoE-lacZ strains) in the presence of NaCl was abolished by glucose, this effect being reversible by cAMP, and there was more NaCl-induced synthesis of this enzyme in relA+ strains. Accordingly, it appears that addition of NaCl to LSB leads to acid sensitivity because it induces synthesis of the OM proton pore PhoE. |
| Links | |
| Keywords |
Escherichia coli/drug effects; Escherichia coli/metabolism; Escherichia coli Proteins; Porins/biosynthesis; Sodium Chloride/pharmacology; beta-Galactosidase/biosynthesis |
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