Mechanism of Action of Nalidixic Acid on
            <i>Escherichia coli</i>
            II. Inhibition of Deoxyribonucleic Acid Synthesis

Goss, William A.; Deitz, William H.; Cook, Thomas M.

doi:10.1128/jb.89.4.1068-1074.1965

Cited by 307 publications

(96 citation statements)

References 8 publications

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“…Fixation itself had no effect on measured anisotropy, and possible direct interactions of drugs with the membrane were excluded by testing with fixed cells (data not shown). Nal inhibits DNA gyrase and, thus, DNA replication (Drlica, 1984), but RNA and protein synthesis can proceed for a while (Goss et al, 1965). The other drugs used here inhibit protein synthesis either directly or eventually (Table 1); in these cases, continued phospholipid synthesis might alter the lipid-protein ratio and perhaps explain the decrease in viscosity.…”

Section: Discussionmentioning

confidence: 98%

“…To detect how nucleoid-membrane interactions are reflected in the membrane dynamics of E. coli, they were altered by inhibiting macromolecular syntheses: DNA replication was inhibited by nalidixic acid (Nal) (Goss et al, 1965;Drlica, 1984), protein synthesis by Cam or Pur and RNA synthesis by Rif (Lark, 1972). Their effects on growth kinetics are well known and are not shown here.…”

Section: Inhibition Of Macromolecular Synthesesmentioning

confidence: 99%

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Transcription‐ and translation‐dependent changes in membrane dynamics in bacteria: testing the transertion model for domain formation

Binenbaum¹,

Parola

Zaritsky³

et al. 1999

Molecular Microbiology

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SummaryCell cycle events have been proposed to be triggered by the formation of membrane domains in the process of coupled transcription, translation and insertion ('transertion') of nascent membrane and exported proteins. Disruption of domain structure should lead to changes in membrane dynamics. Membrane viscosity of Escherichia coli and Bacillus subtilis decreased after inhibition of protein synthesis by chloramphenicol or puromycin, or of RNA initiation by rifampicin, but not after inhibition of RNA elongation by streptolydigin or amino acid starvation of a stringent strain. The decrease caused by inhibitors of protein synthesis was prevented by streptolydigin if added simultaneously, but was not reversed if added later. The drug-induced decrease in membrane viscosity is energy dependent: it did not happen in KCN-treated cells. All treatments decreasing membrane viscosity also induced nucleoid compaction and fusion. Inhibition of macromolecular synthesis without membrane perturbation caused nucleoids to expand. Changes in membrane dynamics were also displayed during a nutritional shift-down transition that causes imbalance in macromolecular syntheses. The results are consistent with the transertion model, predicting dissipation of membrane domains by termination of protein synthesis or detachment of polysomes from DNA; domain structure is conserved if the transertion process is 'frozen'.

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Section: Discussionmentioning

confidence: 98%

Section: Inhibition Of Macromolecular Synthesesmentioning

confidence: 99%

Transcription‐ and translation‐dependent changes in membrane dynamics in bacteria: testing the transertion model for domain formation

Binenbaum¹,

Parola

Zaritsky³

et al. 1999

Molecular Microbiology

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“…The experimental conditions used that partially protected cells from thermally-induced lysis, are known to induce an increase in the amount of some or all of the HSp. However, most of these conditions can also modify the cell cycle by transient arrest of DNA replication (Goss et al 1965).…”

Section: Thermally-induced Lysis Of Cells Aligned For Cell Division Bmentioning

confidence: 99%

Thermally‐induced cell lysis in Escherichia coli K12

Membrillo-Hernández

Mora

Rio-Albrechtsen

et al. 1995

J. Basic Microbiol.

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Escherichia coli cells exposed to high temperatures exhibit a progressive loss of viability. We observed two mechanisms of cell death induced by lethal temperatures: with and without lysis. The number of cells lysed by heat decreased at later stages of the growth curve, when cells were pre-treated at lower temperatures for 10 minutes and when cells were pre-treated with novobiocin, nalidixic acid and cadmium chloride. Cell lysis was similar in wild type, rpoH, groE and dnaK mutant cells as well as in cells which overproduce heat shock proteins GroE or DnaK. Results using cells aligned for cell division and cells growing at 42 degrees C, 45 degrees C and 47 degrees C suggest that cells near division are more sensitive to lysis and that a high concentration of heat-shock proteins increases their resistance to lysis.

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“…Apart from DNA repair, recA and DNA polymerase V (encoded by umuDC) are known to increase spontaneous mutation frequencies resulting in the emergence of antibiotic resistance mutants (Thi et al, 2011). Spontaneous mutation in V. cholerae is well documented to cause resistance to a variety of antibiotics (Goss et al, 1965;Gellert et al, 1977;Sugino et al, 1977;Allen et al, 1979;Kitaoka et al, 2011). Here we chose to examine the mutation frequency of two antibiotics, rifampicin which acts on protein synthesis and nalidixic acid which targets DNA replication by inhibiting the A subunit of DNA gyrase.…”

Section: Resultsmentioning

confidence: 99%

A genomic island integrated into recA of Vibrio cholerae contains a divergent recA and provides multi‐pathway protection from DNA damage

Rapa

Islam²,

Monahan³

et al. 2014

Environmental Microbiology

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Lateral gene transfer (LGT) has been crucial in the evolution of the cholera pathogen, Vibrio cholerae. The two major virulence factors are present on two different mobile genetic elements, a bacteriophage containing the cholera toxin genes and a genomic island (GI) containing the intestinal adhesin genes. Non-toxigenic V. cholerae in the aquatic environment are a major source of novel DNA that allows the pathogen to morph via LGT. In this study, we report a novel GI from a non-toxigenic V. cholerae strain containing multiple genes involved in DNA repair including the recombination repair gene recA that is 23% divergent from the indigenous recA and genes involved in the translesion synthesis pathway. This is the first report of a GI containing the critical gene recA and the first report of a GI that targets insertion into a specific site within recA. We show that possession of the island in Escherichia coli is protective against DNA damage induced by UV-irradiation and DNA targeting antibiotics. This study highlights the importance of genetic elements such as GIs in the evolution of V. cholerae and emphasizes the importance of environmental strains as a source of novel DNA that can influence the pathogenicity of toxigenic strains.

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Mechanism of Action of Nalidixic Acid on Escherichia coli II. Inhibition of Deoxyribonucleic Acid Synthesis

Cited by 307 publications

References 8 publications

Transcription‐ and translation‐dependent changes in membrane dynamics in bacteria: testing the transertion model for domain formation

Transcription‐ and translation‐dependent changes in membrane dynamics in bacteria: testing the transertion model for domain formation

Thermally‐induced cell lysis in Escherichia coli K12

A genomic island integrated into recA of Vibrio cholerae contains a divergent recA and provides multi‐pathway protection from DNA damage

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