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

The Vibrio cholerae acfA, B, C, and D genes are involved in the synthesis of a colonization factor; their expression is under the control of ToxR, the cholera toxin transcriptional activator. By a combination of Southern blot analysis, cloning, and nucleotide sequence analysis, we determined that the acf genes are clustered on a 5-kb region, the acfA and acfD genes are transcribed divergently, and the translation start sites of the two genes are separated by only 173 bp. Expression from the acfA and acfD promoters in V. cholerae was studied by using acfA:phoA translational and acfD-lacZ transcriptional fusions; when carried by the chromosome, the acfA-acfD intergenic region flanked by the two reporter genes was found to contain the cis-acting element(s) necessary for the environmental regulation of the two promoters. However, this regulation was almost completely abolished when the same construction was carried by a low-copy-number plasmid. These results suggested that differences in DNA topology between the plasmid versus the chromosomal constructs might influence the expression of the acfA and acfD promoters. Support for this conclusion was obtained by showing that ToxR-dependent but not basal expression of both promoters was strongly inhibited by nalidixic acid and novobiocin, two DNA gyrase inhibitors, suggesting that the activation of these promoters is affected by changes in DNA supercoiling. Expression of the acfA and acfD promoters was also investigated in the heterologous host Escherichia coli harboring plasmids expressing either ToxR or ToxT, two transcriptional activators of the V. cholerae virulence genes. ToxR activated the acfD promoter 2.5-fold but inhibited the acfA promoter 2-fold. In contrast, the expression of the acfA promoter was activated 10-fold and that of the acfD promoter was activated 3-fold by ToxT, supporting the previously proposed cascade model for organization of the ToxR regulon.
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PMID:Structural analysis of the acfA and acfD genes of Vibrio cholerae: effects of DNA topology and transcriptional activators on expression. 164 47

The sequence (2,700 bp) between the aldH and pspF genes of Escherichia coli was determined. The pspF gene encodes a sigma54 transcriptional activator of the phage shock protein (psp) operon (pspA to pspE). Downstream of the pspF transcribed region are two open reading frames (ORFs), ordL and goaG, convergently oriented with respect to pspF. These two ORFs, together with the adjacent aldH gene, may constitute a novel operon (aldH-ordL-goaG). The goaG-pspF intergenic region contains a complex extragenic mosaic element, RIB. The structure of this RIB element, which belongs to the BIME-1 family, is Y(REP1) > 16 < Z1(REP2), where Y and Z1 are palindromic units and the central 16 bases contain an L motif with an ihf consensus sequence. DNA fragments containing the L motif of the psp RIB element effectively bind integration host factor (IHF), while the Y palindromic unit (REP1) of the same RIB element binds DNA gyrase weakly. Computer prediction of the pspF mRNA secondary structure suggested that the transcribed stem-loop structures formed by the 3'-flanking region of the pspF transcript containing the RIB element can stabilize and protect pspF mRNA. Analysis of pspF steady-state mRNA levels showed that transcripts with an intact RIB element are much more abundant than those truncated at the 3' end by deletion of either the entire RIB element or a single Z1 sequence (REP2). Thus, the pspF 3'-flanking region containing the RIB element has an important role in the stabilization of the pspF transcript.
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PMID:The RIB element in the goaG-pspF intergenic region of Escherichia coli. 915 Feb

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

Mitomycin C (MMC), a DNA-damaging agent, is a potent inducer of the bacterial SOS response; surprisingly, it has not been used to select resistant mutants from wild-type Escherichia coli. MMC resistance is caused by the presence of any of four distinct E. coli genes (mdfA, gyrl, rob, and sdiA) on high-copy-number vectors. mdfA encodes a membrane efflux pump whose overexpression results in broad-spectrum chemical resistance. The gyrI (also called sbmC) gene product inhibits DNA gyrase activity in vitro, while the rob protein appears to function in transcriptional activation of efflux pumps. SdiA is a transcriptional activator of ftsQAZ genes involved in cell division.
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PMID:In vivo titration of mitomycin C action by four Escherichia coli genomic regions on multicopy plasmids. 1124 65