RELEASE OF ULTRAVIOLET-ABSORBING MATERIAL FROM ESCHERICHIA COLI AT SUBZERO TEMPERATURES

1963 ◽  
Vol 9 (4) ◽  
pp. 523-530 ◽  
Author(s):  
Gösta Lindeberg ◽  
Aaslaug Lode
Keyword(s):  
Escherichia Coli ◽  
Nucleic Acids ◽  
Cold Shock ◽  
Organic Phosphorus ◽  
Lethal Effect ◽  
Rapid Cooling ◽  
Pronounced Decrease ◽  
Subzero Temperatures ◽  
Absorbing Material ◽  
Freezing Seawater

When cells of Escherichia coli were suspended in dilute artificial seawater and cooled to various subzero temperatures, a maximum lethal effect occurred around −40 °C. In addition, rapid cooling to −26 °C of bacteria, suspended in concentrated, non-freezing seawater caused a pronounced decrease in viability ("cold shock"). The loss in viability was accompanied by a proportional release from the cells of ultraviolet-absorbing material and by an increase in the ribose and organic phosphorus contents of the suspending liquid. It seems possible that the released material, at least partly, consisted of nucleotides or nucleic acids.

Interaction of Gram-Negative Bacteria with the Lysosomal Fraction of Polymorphonuclear Leukocytes II. Changes in the Cell Envelope of Escherichia coli

1970 ◽  
Vol 1 (3) ◽  
pp. 311-318
Author(s):  
D. Friedberg ◽  
I. Friedberg ◽  
M. Shilo
Keyword(s):  
Escherichia Coli ◽  
Polymorphonuclear Leukocytes ◽  
Cytoplasmic Membrane ◽  
Morphological Changes ◽  
Cell Envelope ◽  
Gram Negative Bacteria ◽  
Intact Cells ◽  
Lysosomal Fraction ◽  
E Coli ◽  
Absorbing Material

Interaction of lysosomal fraction with Escherichia coli caused damage to the cell envelope of these intact cells and to the cytoplasmic membrane of E. coli spheroplasts. The damage to the cytoplasmic membrane was manifested in the release of 260-nm absorbing material and β-galactosidase from the spheroplasts, and by increased permeability of cryptic cells to O -nitrophenyl-β- d -galactopyranoside; damage to the cell wall was measured by release of alkaline phosphatase. Microscope observation showed morphological changes in the cell envelope.

scholarly journals Major cold shock protein of Escherichia coli.

1990 ◽  
Vol 87 (1) ◽  
pp. 283-287 ◽  
Author(s):  
J. Goldstein ◽  
N. S. Pollitt ◽  
M. Inouye
Keyword(s):  
Escherichia Coli ◽  
Cold Shock ◽  
Cold Shock Protein

Perturbation of Growth and Metabolism in Candida albicans by 4-Bromobenzyl Isothiocyanate and Iodoacetate

1973 ◽  
Vol 28 (1-2) ◽  
pp. 21-31 ◽  
Author(s):  
A. Hasilik
Keyword(s):  
Candida Albicans ◽  
Nucleic Acids ◽  
Growth Inhibition ◽  
Cell Suspension ◽  
Lethal Effect ◽  
Thiol Groups ◽  
Early Step ◽  
Additional Information ◽  
Sublethal Doses ◽  
Higher Doses

The inhibition by PBBI of growing Candida albicans was studied; additional information was obtained from the analysis of regeneration. The type of the growth inhibition depended on the cell suspension. At more than 107 cells per ml, the inhibition was transient; the inhibitor was taken up rapidly by the cells to a limit of 37 nmoles per mg dry wet. At higher doses, the growth was inhibited permanently, and then, and only then, a lethal effect was observed. At sublethal doses of the inhibitor, the following effects were observed: Inhibition of respiration without apprecciable .change in R.Q., of incorporation of labelled precursors into proteins and nucleic acids, and of eight of fourteen enzymes studied; the level of total free thiol groups was lowered; and a cross- over between hexose monophosphates and fructose diphosphate was induced. The original activities of the enzymes and metabolic processes inhibited were restored coincidentally with the reappearance of growth of the cells. Inhibition of G-6-PDH, PFK and of an early step in the oxidation of NAD(P)H appeared to be determinative for the growth. In the cells inhibited transiently by iodocetate, GAPDH and ADH were the most sensitive enzymes. The activity of the latter but not of the former was readily restored. The R.Q. was lowered, and was restored later than growth. The cells which recovered from the inhibition by iodoacetate appeared to be physiologically different from the control.

Solution NMR Structure of Ribosome-binding Factor A (RbfA), A Cold-shock Adaptation Protein from Escherichia coli

2003 ◽  
Vol 327 (2) ◽  
pp. 521-536 ◽  
Author(s):  
Yuanpeng Janet Huang ◽  
G.V.T. Swapna ◽  
P.K. Rajan ◽  
Haiping Ke ◽  
Bing Xia ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Cold Shock ◽  
Nmr Structure ◽  
Solution Nmr ◽  
Ribosome Binding ◽  
Binding Factor

scholarly journals Cold Shock Induces Chromosomal qnr in Vibrio Species and Plasmid-Mediated qnrS1 in Escherichia coli

2019 ◽  
Vol 63 (12) ◽  
Author(s):  
Hee-Chang Jang ◽  
Yin Wang ◽  
Chunhui Chen ◽  
Laura Vinué ◽  
George A. Jacoby ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Bacterial Community ◽  
Vibrio Parahaemolyticus ◽  
Cold Shock ◽  
Vibrio Vulnificus ◽  
Wild Type ◽  
Induced Expression ◽  
Content Type ◽  
E Coli ◽  
Dna Damaging Agents

ABSTRACT qnr genes are found in aquatic bacteria and were present in the bacterial community before the introduction of synthetic quinolones. Their natural functions are unknown. We evaluated expression of chromosomal qnr in Vibrio species in response to environmental stresses and DNA-damaging agents. Subinhibitory concentrations of quinolones, but not other DNA-damaging agents, increased expression of chromosomal qnr by more than five times in Vibrio parahaemolyticus, Vibrio vulnificus, and Vibrio mytili. Cold shock also induced expression of qnr in V. parahaemolyticus, V. vulnificus, and V. mytili, as well as expression of qnrS1 in Escherichia coli. qnrS1 induction by cold shock was not altered in ΔihfA or ΔihfB mutants or in a strain overexpressing dnaA, all of which otherwise directly modulate qnrS1 induction by ciprofloxacin. In contrast, the level of qnrS1 induction by cold shock was reduced in a ΔcspA mutant in the cold shock regulon compared to the wild type. In conclusion, cold shock and quinolones induce expression of chromosomal qnr in Vibrio species and of the related qnrS1 gene in E. coli.

scholarly journals The Extracellular Death Factor: Physiological and Genetic Factors Influencing Its Production and Response in Escherichia coli

2008 ◽  
Vol 190 (9) ◽  
pp. 3169-3175 ◽  
Author(s):  
Ilana Kolodkin-Gal ◽  
Hanna Engelberg-Kulka
Keyword(s):  
Escherichia Coli ◽  
Cell Death ◽  
Genetic Factors ◽  
Strain Differences ◽  
Lethal Effect ◽  
Mixed Population ◽  
Signal Molecule ◽  
Physiological Conditions ◽  
Dehydrogenase Gene ◽  
Glucose 6 Phosphate Dehydrogenase

ABSTRACT Gene pairs specific for a toxin and its antitoxin are called toxin-antitoxin modules and are found on the chromosomes of many bacteria. The most studied of these modules is Escherichia coli mazEF, in which mazF encodes a stable toxin, MazF, and mazE encodes a labile antitoxin, MazE, which prevents the lethal effect of MazF. In a previous report from this laboratory, it was shown that mazEF-mediated cell death is a population phenomenon requiring a quorum-sensing peptide called the extracellular death factor (EDF). EDF is the linear pentapeptide NNWNN (32). Here, we further confirm that EDF is a signal molecule in a mixed population. In addition, we characterize some physiological conditions and genes required for EDF production and response. Furthermore, stress response and the gene specifying MazEF, the Zwf (glucose-6-phosphate dehydrogenase) gene, and the protease ClpXP are critical in EDF production. Significant strain differences in EDF production and response explain variations in the induction of mazEF-mediated cell death.

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