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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A temperature-sensitive mutant of E. coli with a defective DNA gyrase B subunit has been obtained. The mutation is expressed in the thermolability of DNA gyrase in vitro and in DNA relaxation in vivo. DNA replication in the mutant does not stop under non-permissive conditions; its rate gradually falls by a factor of 2 to 3. The transcription rate also drops by a factor of 2 to 3, but before replication. Small concentrations of rifampicin, an inhibitor of bacterial RNA polymerase, make for a partial survival of the mutant cells under non-permissive conditions. The results suggest the conclusion that DNA supercoiling is mainly required to ensure the optimum transcription level in the cell.
Mol Gen Genet 1982
PMID:DNA replication and transcription in a temperature-sensitive mutant of E. coli with a defective DNA gyrase B subunit. 629 83

We have noted previously that when circular, but not linear, DNA or chromatin was injected into Xenopus laevis oocytes, much of it went through an intermediate form in which it did not readily enter an agarose gel; after a few hours, it reappeared as monomer DNA that had acquired its full complement of nucleosomes (T. J. Miller and J. E. Mertz, Mol. Cell. Biol. 2:1581-1593, 1982). We determined, using electron microscopy and a variety of biochemical techniques, the structure of this aggregated material. Most of it was oligomeric and multimeric catenanes of the injected sample. In addition, injection of DNA that had been catenated in vitro with DNA gyrase resulted in the conversion of most of it back to monomer circles. These findings demonstrate directly that both catenation and decatenation of DNA occur in vivo under physiological conditions. Whether these reactions play a crucial role in nucleosome formation, as well as in DNA replication and recombination, remains to be determined.
Mol Cell Biol 1983 Jan
PMID:In vivo catenation and decatenation of DNA. 629 3

We have previously shown that DNA gyrase of Escherichia coli can promote recombination between heterologous DNAs in a cell-free system (Ikeda et al. 1982). In the present paper, we have studied the nucleotide sequences of several recombination junctions of lambda-pBR322 recombinants and found that there were not more than three-basepair homologies between the parental DNAs in six combinations of the lambda and pBR322 recombination sites. Based on this and previous results, we concluded that homology was not required for the DNA gyrase-mediated recombination. Furthermore, the structures of the recombinant DNAs we have analyzed suggest the occurrence of multiple cross-overs in our in vitro system.
Mol Gen Genet 1984
PMID:Homology is not required for recombination mediated by DNA gyrase of Escherichia coli. 631 62

Bacteriophage Mud (Casadaban and Cohen 1979) was used to bring the transcription of the gene for beta galactosidase (lacZ) under the control of the promoter of the structural gene for colicin Ib (cia(Ib)) on a derivative of the Col plasmid Col-Ib.P9. Transcription of this fusion operon was stimulated by agents which damaged cellular DNA (mitomycin C, bleomycin and colicin E2). Increased transcription of the cia-lacZ operon could be detected within 13 min of the addition of these agents. In a strain bearing the tif-1 (recA441) mutation, constitutive expression of the SOS DNA repair system at 42 degree C also increased transcription of the cia-lacZ operon. Transcription of the cia-lacZ operon was also stimulated by inhibition of DNA gyrase activity with nalidixic acid but not with novobiocin. Transitory inhibition of protein synthesis with chloramphenicol or by proline starvation of a proline auxotroph did not stimulate cia-lacZ transcription. Transcription of the cia-lacZ operon was substantially reduced in the presence of a recA mutation, but was largely unaffected by a mutation in recB affecting the RecBC DNase or by catabolite repression. Control experiments in which the production of colicin Ib was measured confirmed that the experiments with the fusion operon gave an accurate indication as to the activity of the wild type cia gene except for the effect of catabolite repression, where we observed up to 99% reduction in colicin Ib production in strains carrying mutant crp or cya alleles. The overall results confirm previous suggestions that there was considerable similarity between the regulatory systems controlling production of colicins and the repressor-dependent regulation of lambdoid prophage induction.
Mol Gen Genet 1981
PMID:Transcription regulation of colicin Ib synthesis. 646 Sep 13

Low concentrations of the antibiotic coumermycin A1, the inhibitor of bacterial DNA gyrase, effectively eliminate pBR322, pMB9 and other ColE 1 related plasmids from E. coli K12 strains. The curing action of antibiotic seems to result from the plasmid degradation and not just from the inhibition of replication.
Mol Gen Genet 1980 Apr
PMID:Curing of Escherichia coli K12 plasmids by coumermycin. 699 78

Chromosome replication cycle in a DNA initiation mutant of Escherichia coli (CRT-83, dnaAts) was blocked by nalidixic acid, an inhibitor of the A subunit of DNA gyrase. Following a period of inhibition of DNA synthesis, the drug was removed and "run-out" DNA synthesis was examined. It was found that the "capacity" for DNA synthesis was not affected by such a treatment.
Mol Gen Genet 1981
PMID:Chromosome replication following a temporary inhibition of DNA-synthesis by nalidixic acid in a temperature-sensitive dnaA mutant of Escherichia coli. 701 51

Clorobiocin, an inhibitor of the gyrB subunit of DNA gyrase, was used for the curing of some Escherichia coli plasmids. Of the plasmids studied, ampicillin resistant R28K and a miniplasmid derived from R1drd-19 were effectively eliminated. We also succeeded in eliminating the ColA factor from E. coli strain B834(pBS103), which was resistant to the effect of currently used curing agents. Although a derivative of ColE1-pBR322 was effectively cured by clorobiocin, the ColE1 plasmid was resistant to its effect. The ColV plasmid determining virulence was effectively eliminated.
Mol Gen Genet 1982
PMID:Curing effect of clorobiocin on Escherichia coli plasmids. 705 Jun 23

Induction of supercoiling in plasmid DNA by HU heterotypic and homotypic dimers, a mutant HU-2 (HupAN12), HBs and HB1 proteins with different DNA-binding affinities was investigated in vitro. The abilities of these proteins to induce supercoiling in DNA correlated with their affinities for DNA. Stoichiometrical analysis of HU heterodimers bound to DNA in the complex restraining the negative torsional tension of DNA showed that 12-13 dimers account for a single superhelical turn. The number of supercoils in the plasmid in vivo decreased on inhibition of DNA gyrase with coumermycin, reaching a steady-state level that indicated the existence of a compartment of restrained supercoils. The size of the restrained compartment was reduced in the absence of HU, indicating the participation of HU in constituting this fraction, and was larger on overproduction of HU-2 in the cells. An increased level of DNA gyrase, expressed from a plasmid carrying both gyr genes, in the cells did not compensate for the deficit of the restrained supercoils caused by HU deficiency, indicating seeming distinct and unrelated action of HU and DNA gyrase in introducing and constraining supercoiling of intracellular DNA.
Mol Gen Genet 1995 Sep 20
PMID:Role of HU proteins in forming and constraining supercoils of chromosomal DNA in Escherichia coli. 747 50

Bacterial plasmids are stabilized by a number of different mechanisms. Here we describe the molecular aspects of a group of plasmid-encoded gene systems called the proteic killer gene systems. These systems mediate plasmid maintenance by selectively killing plasmid-free cells (post-segregational killing or plasmid addiction). The group includes ccd of F, parD/pem of R1/R100, parDE of RP4/RK2, and phd/doc of P1. All of these systems encode a stable toxin and an unstable antidote. The antidotes prevent the lethal action of their cognate toxins by forming tight complexes with them. The antidotes are degraded by cellular proteases. Thus, the different decay rates of the toxins and antidotes seem to be the molecular basis of toxin activation in plasmid-free cells. The operons encoding the toxins and antidotes are autoregulated at the level of transcription either by a complex formed by the toxins and the cognate antidotes or by the antidote alone. The cellular targets of the killer proteins have been determined to be DNA gyrase in the case of ccd of F and DnaB in the case of parD of R1. Surprisingly, the Escherichia coli chromosome encodes at least two of these peculiar gene systems.
Mol Microbiol 1995 Jul
PMID:Programmed cell death in bacteria: proteic plasmid stabilization systems. 749 69

A spontaneously occurring, nalidixic acid-resistant (NalR), thermotolerant (T/r) mutant of Escherichia coli was isolated. Bacteriophage P1-mediated transduction showed that NalR mapped at or near gyr A, one of the two genes encoding DNA gyrase. Expression of gyrA+ from a plasmid rendered the mutant sensitive to nalidixic acid and to high temperature, the result expected for alleles mapping in gyrA. Plasmid linking number measurements, made with DNA from cells grown at 37 degrees C or shifted to 48 degrees C, revealed that supercoiling was about 12% less negative in the T/r mutant than in the parental strain. Each strain preferentially expressed two different proteins at 48 degrees C. The genetic and supercoiling data indicate that thermotolerance can arise from an alteration in DNA gyrase that lowers supercoiling. This eubacterial study, when coupled with those of archaebacteria, suggests that DNA relaxation is a general aspect of thermotolerance.
Mol Gen Genet 1995 Aug 30
PMID:DNA supercoiling in a thermotolerant mutant of Escherichia coli. 756 5


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