Chloramphenicol Inhibition of Polyuridylic Acid Binding to E. coli Ribosomes

Jardetzky, Oleg; Julian, Gordon R.

doi:10.1038/201397a0

Cited by 47 publications

(9 citation statements)

References 7 publications

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“…The growth of large peptides on ribosomes from a CM-sensitive strain in the presence of CM is inhibited, whereas the synthesis of di-and tripeptides is not inhibited, leading to the suggestion that CM interferes with peptide bond-forming enzymes (9). This is in contrast to the suggestion that CM inhibits attachment of messenger ribonucleic acid (mRNA) to the ribosome (8).…”

Section: Discussioncontrasting

confidence: 78%

Effect of Resistance to Chloramphenicol on Bacteriophage Sensitivity of Group A Streptococci

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Slade

1967

J Virol

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Several phage hosts of group A streptococci became resistant to lysis by bacteriophage as a consequence of having acquired the ability to grow in the presence of chloramphenicol. The phage was adsorbed to the streptococcal cell, and P 32 -labeling of the phage showed that the phage genome penetrated the chloramphenicol (CM)- resistant cells as it did the parent cells. However, artificial lysis of the infected CM-resistant cells with chloroform or enzymes revealed no intracellular mature phage particles. Lysates of infected CM-resistant cells contained no phage-related antigenic materials which possessed serum-blocking power, although they were readily detected in lysates of infected parent cells. The CM-resistant cells were not lysogenized by the phage. Only cells resistant to more than 10 μg/ml of chloramphenicol were resistant to phage, and this threshold effect was taken as an indication of at least two different loci of chloramphenicol resistance on the streptococcal genome. Strains resistant to high levels of other antibiotics, such as streptomycin and erythromycin, showed no resistance to lysis by phage. Evidence indicated that the mutant cells were deficient in an essential function associated with the phage genome.

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Section: Discussioncontrasting

confidence: 78%

Effect of Resistance to Chloramphenicol on Bacteriophage Sensitivity of Group A Streptococci

Friend

Slade

1967

J Virol

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“…The RNA moiety (chloramphenicol-RNA) has been thought to resemble messenger RNA in some respects (14)(15)(16), and on this basis, Rendi & Ochoa (17) suggested that chloramphenicol might interfere with the attachment of messenger RNA to ribosomes. In support of this hypothesis, J ardetzky & Julian were able to demonstrate that chlor amphenicol partially inhibited the binding of C14-polyuridylic acid to E. coli ribosomes in vitro (18). On the basis of nuclear magnetic resonance studies, Jardetzky proposed that competition for ribosomal binding sites might be related to a conformational similarity between chloramphenicol and pyrim idine nucleotides (19).…”

Section: Inhibition Of Microbial Protein Synthesis By Chloramphenicolmentioning

confidence: 94%

Inhibition of Protein Synthesis by Chloramphenicol

Weisberger¹

1967

Annu. Rev. Med.

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“…The attachment of phenylalanyl transfer RNA to the poly U-ribosomes complex was not inhibited by chloramphenicol (NAKAMOTO et al, 1963;jARDETZKY and jULIAN, 1964;SUAREZ and NATHANS, 1965) but WoLFE and HAHN reported (1965) a stereospecific inhibition by chloramphenicol (3 x 1 o-4 M) of the poly A-directed binding of lysyl transfer RNA to ribosomes. While the low magnitude of this effect ( 1 Q--15 %) appeared to rule it out as an explanation of the strong action of the antibiotic on the lysine incorporation system as recorded by SPEYER et al ( 1963), the subsequent finding of that the antibiotic (2.1 x 1Q-4 M) actually inhibits peptide bond synthesis in this system by only 23 % has rendered the observation of WOLFE and HAHN more significant.…”

Section: Chloramphenicol 315mentioning

confidence: 95%

Antibiotics

1967

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AII rights, especially that of tnmslation into foreign languages, reserved. It is also forbidden to reproduce this book, either whole DedicationFor most areas of scientific pursuit, there is usually that rare investigator who has the imagination to conceive ideas, who has faith in his visions, and who has the ability to critically test his concepts in the laboratory. Almost invariably, this scientist also inspires younger men to enthusiastically enter into his research program. To him should go the accolades and the recognitions of the esteem in which he is held. As only a small part of this esteem, we wish to dedicate these books to Professor SELMAN A. W AKSMAN in appreciation of his leadership and contributions in all facets of antibiotic research. PrefaceThe idea for publishing these books on the mechanism of action and on the biosynthesis of antibiotics was born of frustration in our attempts to keep abreast of the literature. Gone were the years when we were able to keep a bibliography on antibiotics and feel confident that we could find everything that was being published on this subject. These fields of investigation were moving forward so rapidly and were encompassing so wide a range of specialized areas in microbiology and chemistry that it was almost impossible to keep abreast of developments. In our naivete and enthusiasm, however, we were unaware that we were toying with an idea that might enmesh us, that we were creating an entity with a life of its own, that we were letting loose a Golom who instead of being our servant would be our master.That we set up ideals for these books is obvious; they would be current guides to developments and information in the areas of mechanism of action and biosynthesis of antibiotics. For almost every subject, we wished to enlist the aid of an investigator who himself had played a part in determining the nature of the phenomena that were being discussed. One concept for the books was that they include only antibiotics for which a definitive, well-documented mechanism of action or biosynthetic pathway was known. Yet, such an approach would not entirely serve the purpose we projected, for it would not encompass all of the information available in these fields of antibiotic investigations and blind searches for the original literature would still have to be made. We therefore chose to include any and all antibiotics about which some pertinent information had been published. It was obvious even at the start that such a compilation, integration, and analysis of information could never be complete unless scientific investigations ceased at the moment the last manuscript was submitted-an end that was neither desirable nor possible. An addendum was therefore included at the end of the volume and left open for the addition of new information until the last pages of the regular articles had been printed.The original concept has also been further expanded as the authors of several papers found it advisable to elaborate on their subject. Some of the articles included discussions...

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Chloramphenicol Inhibition of Polyuridylic Acid Binding to E. coli Ribosomes

Cited by 47 publications

References 7 publications

Effect of Resistance to Chloramphenicol on Bacteriophage Sensitivity of Group A Streptococci

Effect of Resistance to Chloramphenicol on Bacteriophage Sensitivity of Group A Streptococci

Inhibition of Protein Synthesis by Chloramphenicol

Antibiotics

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