The role of regulatory gene products in alkali sensitization by extracellular medium components in Escherichia coli

Abstract

become alkali sensitized on transfer from pH 7·0 to pH 5·5 but they also secrete extracellular agents which induce alkali sensitivity when added (in neutralized filtrates) to organisms growing at pH 7·0. In contrast, filtrates from cultures grown at pH 7·0 have no effect. Filtrates were inactivated by protease but not by heat treatment in a boiling water-bath, suggesting that a very heat-stable protein is involved in alkali sensitivity induction. A heatstable low molecular weight component (or components) may also be needed for induction, or the induction protein itself may be of low molecular weight. Strains with lesions in hns, fur or himA produced almost inactive filtrates and it therefore appears that H-NS, Fur and IHF are involved in synthesis of the induction components. As the presence of protease during incubation at pH 5·5 totally abolished alkali sensitization of strain 1829 while inhibition of sensitization induction occurred if the induction components were removed by filtration or dialysis during pH 5·5 incubation, it is proposed that the extracellular induction components (EICs) are essential for the original sensitization response. These results suggest that sensitization induction occurs by a different mechanism to that which is believed to occur for most bacterial inducible response systems; these are claimed to involve exclusively intracellular reactions and components whereas the present response involves functioning of extracellular components.

Properties of an L‐glutamate‐induced acid tolerance response which involves the functioning of extracellular induction components

“…1989 ). Such inhibition occurs for the recently reported acid tolerance response induced at pH 7·0 by glucose ( Rowbury & Goodson 1998b). In contrast, nalidixic acid had no inhibitory effect on induction of the l ‐glutamate‐induced acid tolerance ( Table 1).…”

“…It has recently been established that induction of several stress tolerance responses involves the functioning of extracellular components ( Hussain et al . 1998 ; Rowbury & Goodson 1998a, b), i.e. components in medium filtrates.…”

“…The l ‐glutamate‐induced acid tolerance described here is one of a number of such tolerance responses known to be induced in log‐phase organisms at neutral pH. That induced by glucose (the glucose response) has been studied in some detail ( Rowbury & Goodson 1998b) but the present response, and that induced by glucose, are quite distinct in that the former response is markedly more sensitive to inhibition by cAMP than is the latter, while the glucose response is sensitive to inhibition by nalidixic acid (Nal) whereas the l ‐glutamate response is not ( Table 1). The absence of any effect of Nal on the l ‐glutamate response suggests that induction is not appreciably affected by the extent of supercoiling in the region of the DNA encoding the tolerance genes.…”

“…1990 ). In contrast, several stress tolerance responses are now known to involve the obligate functioning of extracellular induction components and extracellular sensors ( Rowbury & Goodson 1998a, b; Rowbury & Hussain 1998). Stress tolerance responses are possibly an unusual group of inducible processes, but if not, ideas on how inducible processes in general are switched on may have to be re‐examined.…”

An extracellular stress‐sensing protein is activated by heat and u.v. irradiation as well as by mild acidity, the activation producing an acid tolerance‐inducing protein

“…Until recently, it had seemed highly likely that the process for switching‐on stress responses was similar to the above in that the sensor for the EnvZ/OmpR system which responds to osmotic stress (the sensor is the EnvZ protein of the cytoplasmic membrane) and the subsequent reactions and components involved in switching‐on the response (changes in OmpF/OmpC levels) are all intracellular. Recent findings have, however, established that for many pH responses, there are extracellular components essential for induction ( Rowbury & Goodson 1998; Rowbury & Hussain 1998; Rowbury 1998). The present work shows that the sensor for one such response is an extracellular protein which responds to mild acidity, to mild heat and to u.v.…”