Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P51532 (transcriptional activator)
 6,546 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 Fe3+, Fe2+, glucose/cAMP or by lrp, him, fur, hns or nhaA/B lesions. Alkali tolerance (habituation), induced at pH0 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 pH0 9.0. Alkali sensitivity induced at pH0 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), FeCl3 and hns and relA lesions, the effect of relA being envZ-suppressed. Acid sensitivity induction (ASI) at pH0 9.0 needs H-NS, is inhibited by FeCl3 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 Fe3+, Fe2+, tetracycline, glucose and nalidixic acid, but not by chloramphenicol; increased outer membrane proton passage may result from OmpA modification.
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PMID:Regulatory components, including integration host factor, CysB and H-NS, that influence pH responses in Escherichia coli. 917 36

Lrp is a global regulator of metabolism in Escherichia coli that helps cells respond to changes in environmental conditions. The action of Lrp as a transcriptional activator or repressor is sometimes affected by whether the medium contains exogenous leucine. The abundance of Lrp in cells is relatively high (about 15 microM in monomer), and given the relatively high Lrp binding affinity in vitro for specific binding sites (nanomolar apparent dissociation constants), the expectation is that all binding sites will be saturated with Lrp in vivo. Here we consider the fraction of the total Lrp in cells that is free and the fraction that is bound to DNA. Using minicell-producing strains, we measured the distribution of Lrp between cytoplasm and nucleoid in cells grown under different nutritional conditions and in cells in different phases of growth. In E. coli cells grown in minimal medium to mid-log phase, the ratio of free to DNA-bound Lrp was about 0.67. This ratio decreased about threefold when the cells were grown in minimal medium supplemented with leucine. Our results also confirmed the previous finding that growth rate regulates lrp expression by as much as three to fourfold. Growth rate-regulated lrp expression, along with changes in the extent of non-specific binding, influences the level of free Lrp in vivo over a 16-fold range. We propose that the net effect of these processes is to regulate the relative concentrations of free Lrp hexadecamer and leucine-bound octamer, leading to promoter selection in response to environmental conditions.
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PMID:Modulation of Lrp action in Escherichia coli by leucine: effects on non-specific binding of Lrp to DNA. 1174 23

Host-encoded functions that regulate the transfer operon (tra) in the virulence plasmid of Salmonella enterica (pSLT) were identified with a genetic screen. Mutations that decreased tra operon expression mapped in the lrp gene, which encodes the leucine-responsive regulatory protein (Lrp). Reduced tra operon expression in an Lrp- background is caused by lowered transcription of the traJ gene, which encodes a transcriptional activator of the tra operon. Gel retardation assays indicated that Lrp binds a DNA region upstream of the traJ promoter. Deletion of the Lrp binding site resulted in lowered and Lrp-independent traJ transcription. Conjugal transfer of pSLT decreased 50-fold in a Lrp- background. When a FinO- derivative of pSLT was used, conjugal transfer from an Lrp- donor decreased 1000-fold. Mutations that derepressed tra operon expression mapped in dam, the gene encoding Dam methyltransferase. Expression of the tra operon and conjugal transfer remain repressed in an Lrp- Dam- background. These observations support the model that Lrp acts as a conjugation activator by promoting traJ transcription, whereas Dam methylation acts as a conjugation repressor by activating FinP RNA synthesis. This dual control of conjugal transfer may also operate in other F-like plasmids such as F and R100.
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PMID:Conjugal transfer of the virulence plasmid of Salmonella enterica is regulated by the leucine-responsive regulatory protein and DNA adenine methylation. 1206 46