Premium
Regulatory components, including integration host factor, CysB and H‐NS, that influence pH responses in Escherichia coli [Note 1. Dedication : This review is dedicated to Dr Rohan G. ...]
Author(s) -
Rowbury R. J.
Publication year - 1997
Publication title -
letters in applied microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.698
H-Index - 110
eISSN - 1472-765X
pISSN - 0266-8254
DOI - 10.1046/j.1472-765x.1997.00065.x
Subject(s) - lysine decarboxylase , dna gyrase , escherichia coli , biochemistry , dna supercoil , dna , lysine , antiporter , biology , activator (genetics) , chemistry , biophysics , amino acid , dna replication , gene , membrane , enzyme , cadaverine , putrescine
This review describes a range of pH responses. Some are only induced if relevant DNA is brought to an appropriately supercoiled configuration by DNA gyrase and bent by the action of, for example, integration host factor (IHF). Bending may allow transcription by bringing activators into juxtaposition with RNA polymerase, which is CysB‐associated in several of the responses. Control of arginine decarboxylase (AdiA) synthesis at acid pH is of the above type, with dependence on the presence of gyrase, H‐NS, IHF and CysB ; acid induction of LysU has similar requirements but also needs Lrp ; lysine decarboxylase (CadA) formation at acid pH is controlled quite differently, needing the CadC activator and interaction of lysine/lysine permease ; H‐NS probably reverses induction by CadC. The Hyd components of formic hydrogenlyase are induced by acid under anaerobiosis ; a transcriptional activator is involved and Fur may also function in regulation. Acid tolerance induced at low pH in log‐phase cells needs CysB and PhoE but not DNA gyrase ; tolerance is reduced by NaCl but not affected by Fe 3+ , Fe 2+ glucose/cAMP or by lrp , him , fur , hns or nhaA / B lesions. Alkali tolerance (habituation), induced at pH 0 8·5–9·0, probably involves DNA supercoiling and bending ; the induction process needs IHF, CysB, PhoE, NhaA, TonB and Fur and is glucose‐repressed ; tolerance may result from Na + efflux catalysed by the NhaA antiporter, which is induced at pH 0 9·0. Alkali sensitivity induced at pH 0 5·5 also requires gyrase, IHF and CysB, but H‐NS, Lrp, NhaA and OmpC are also needed and induction is abolished by NaCl. Salt‐induced acid sensitivity results from PhoE formation and is blocked by glucose (reversed by cAMP), FeCl 3 and hns and relA lesions, the effect of relA being envZ ‐suppressed. Acid sensitivity induction (ASI) at pH 0 9·0 needs H‐NS, is inhibited by FeCl 3 and amiloride, and is associated with alkyl hydroperoxide reductase synthesis. Leucine‐induced acid sensitivity needs gyrase, CysB, H‐NS, Fur, OmpA and RelA, is inhibited by Fe 3+ , Fe 2+ , tetracycline, glucose and nalidixic acid, but not by chloramphenicol ; increased outer membrane proton passage may result from OmpA modification.