Reversal of L-cycloserine inhibition of nucleic acid and protein synthesis by L-alanine in Escherichia coli

1961 ◽  
Vol 26 (6) ◽  
pp. 1729-1731 ◽  
Author(s):  
D. Grünberger ◽  
V. F. Hess ◽  
F. Šorm
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Nucleic Acid

scholarly journals Flow Cytometric Investigation of Filamentation, Membrane Patency, and Membrane Potential in Escherichia coli following Ciprofloxacin Exposure

2000 ◽  
Vol 44 (3) ◽  
pp. 682-687 ◽  
Author(s):  
H. J. Wickens ◽  
R. J. Pinney ◽  
D. J. Mason ◽  
V. A. Gant
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Cell Division ◽  
Membrane Potential ◽  
Nucleic Acid ◽  
Nutrient Broth ◽  
Nucleic Acid Binding ◽  
Dye Uptake ◽  
Flow Cytometric ◽  
Drug Removal

ABSTRACT Ninety-eight percent of the cells in a population ofEscherichia coli in log-phase growth lost colony-forming ability after being exposed for 3 h to the quinolone antibiotic ciprofloxacin at four times the MIC in nutrient broth, a concentration easily reached in vivo. Flow cytometric analysis, however, demonstrated that only 68% of this bacterial population had lost membrane potential, as judged by the membrane potential-sensitive dye bis-(1,3-dibutylbarbituric acid) trimethine oxonol [DiBAC4(3)], and only 30% could no longer exclude the nucleic acid-binding dye propidium iodide (PI), reflecting lost membrane integrity, efflux mechanisms, or both. Subsequent removal of ciprofloxacin and resuspension in nutrient broth resulted in renewed cell division after 2 h, with a calculated postantibiotic effect (PAE) time of 57 min. The proportion of DiBAC- and PI-fluorescent cells in this recovering population remained stable for more than 4 h after antibiotic removal. Eighty percent of cells present at drug removal were filamentous. Their number subsequently decreased with time, and the increase in particle count seen at the end of the PAE resulted from the division of short cells. Exposure to ciprofloxacin in the presence of the protein synthesis inhibitor chloramphenicol increased colony-forming ability to 60% of starting population numbers. In contrast to ciprofloxacin alone, this antibiotic combination resulted in insignificant filamentation and no dye uptake. Subsequent drug removal and resuspension in nutrient broth resulted in the appearance of filaments within 1 h, with 69% of the population forming filaments at 3 h. Dye uptake was also seen, with 20% of the population fluorescing with either dye after 4 h. We were unable to relate dye uptake to the viable count. Cell division resumed 240 min after removal of both drugs, yielding a PAE calculated at 186 min. Inhibition of protein synthesis with chloramphenicol prevented ciprofloxacin-induced changes in bacterial morphology, cell membrane potential, and ability to exclude nucleic acid-binding dye. These changes persisted beyond the end of the classically defined PAE and were not a definite indicator of cell death as defined by loss of colony formation, which related at least in part to filamentation.

THE EFFECT OF ACTINOBOLIN ON NUCLEIC ACID AND PROTEIN SYNTHESIS IN ESCHERICHIA COLI

1966 ◽  
Vol 12 (3) ◽  
pp. 515-520 ◽  
Author(s):  
D. E. Hunt ◽  
R. F. Pittillo ◽  
E. P. Johnson ◽  
F. C. Moncrief
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis ◽  
Amino Acid ◽  
Nucleic Acid ◽  
Mechanism Of Action ◽  
Rna Synthesis ◽  
The Other ◽  
Cross Resistance ◽  
Inhibition Of Protein Synthesis

Actinobolin inhibits protein synthesis in Escherichia coli. When the antibiotic is added to a culture at the time of inoculation, RNA synthesis is also inhibited. Inhibition of RNA synthesis appears to be a consequence of inhibition of protein synthesis. Cross-resistance experiments suggest that the mechanism of action of actinobolin differs from that of the other inhibitors of protein synthesis, chloramphenicol and sparsomycin. Phenylalanine prevents the action of actinobolin provided the amino acid and antibiotic are added simultaneously; this effect is not observed if the phenylalanine is added 1 hour after the addition of the antibiotic. Evidence is presented that the mechanism by which phenylalanine prevents inhibition by actinobolin differs from that which has been suggested for azaserine and p-fluorophenylalanine.

Infection of Escherichia coli with bacteriophages

1969 ◽  
Vol 27 ◽  
pp. 370-371
Author(s):  
Manfred E. Bayer
Keyword(s):  
Escherichia Coli ◽  
Nucleic Acid ◽  
Cell Surface ◽  
Virus Type ◽  
Infection Process ◽  
Adsorption Site ◽  
The Other ◽  
Specific Receptors ◽  
Bacterial Receptors

The first step in the infection of a bacterium by a virus consists of a collision between cell and bacteriophage. The presence of virus-specific receptors on the cell surface will trigger a number of events leading eventually to release of the phage nucleic acid. The execution of the various "steps" in the infection process varies from one virus-type to the other, depending on the anatomy of the virus. Small viruses like ØX 174 and MS2 adsorb directly with their capsid to the bacterial receptors, while other phages possess attachment organelles of varying complexity. In bacteriophages T3 (Fig. 1) and T7 the small conical processes of their heads point toward the adsorption site; a welldefined baseplate is attached to the head of P22; heads without baseplates are not infective.

scholarly journals Control of Protein Synthesis in Escherichia coli

1974 ◽  
Vol 249 (19) ◽  
pp. 6280-6287 ◽  
Author(s):  
Kathleen Crist Westover ◽  
Lewis A. Jacobson
Keyword(s):  
Escherichia Coli ◽  
Protein Synthesis
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