Polyribosome metabolism in Escherichia coli treated with chloramphenicol, neomycin, spectinomycin or tetracycline

Gurgo, Corrado; Apirion, David; Schlessinger, David

doi:10.1016/0022-2836(69)90100-4

Cited by 72 publications

(27 citation statements)

References 29 publications

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“…The present data do not substantiate the uncoupling model for CAP proposed by Gurgo et al (3). Since uncoupling would presumably begin immediately upon the addition of CAP to a culture, one would expect that incomplete protein fragments would accumulate.…”

Section: Resultscontrasting

confidence: 99%

“…Gurgo et al (3) have therefore suggested that CAP uncouples ribosomal movement from protein synthesis because it allows the continued formation of nonfunctional polysomes in the absence of protein synthesis. On the other hand, other investigators (1,10) have demonstrated that nascent peptides could be trapped in the polysome region by high concentrations of CAP, indicating that such uncoupling does not occur.…”

mentioning

confidence: 99%

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Recovery of Polysome Function of T4-Infected Escherichia coli After Brief Treatment with Chloramphenicol and Rifampin

Green¹,

Cameron

Julian³

1975

Antimicrob Agents Chemother

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T4-infected Escherichia coli cells briefly exposed to rifampin, or to rifampin plus chloramphenicol, were capable of protein synthesis for some time after removal of the antibiotics, although ribonucleic acid synthesis was irreversibly inhibited. Partially completed peptides trapped on polysomes by high levels of chloramphenicol were eventually completed after removal of the drug, as demonstrated by subjecting labeled peptides from appropriate polysome regions to polyacrylamide disc gel electrophoresis. Thus, the effect of the drug appears to be reversible on the molecular as well as the cellular level.

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Section: Resultscontrasting

confidence: 99%

mentioning

confidence: 99%

Recovery of Polysome Function of T4-Infected Escherichia coli After Brief Treatment with Chloramphenicol and Rifampin

Green¹,

Cameron

Julian³

1975

Antimicrob Agents Chemother

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“…8d) becomes more pronouncedly curved, as would be expected if there were at least partial interactions between the CAPr and CAPS genomes, with the latter being dominant. However, a dominance of the CAPS allele would be in contrast to the available evidence from bacterial systems indicating that the CAPS ribosomes are not "frozen" by CAP on the polysomes and are therefore not expected to block the passage of the resistant ones (18); also, the well-documented isolation of CAPr mutants of Saccharomyces cerevisiae (4, 7) and mammalian cells (44,48) under selective conditions, which would require the initial expression of single mutant mtDNA molecules mixed with wild-type molecules, argues strongly against a dominance of the CAPS allele. Therefore, the data are most consistent with the conclusion that the CAPr and CAPS genomes in these cybrids are phenotypically independent.…”

Section: Resultsmentioning

confidence: 71%

Complementation of mutant and wild-type human mitochondrial DNAs coexisting since the mutation event and lack of complementation of DNAs introduced separately into a cell within distinct organelles.

1994

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The rules that govern complementation of mutant and wild-type mitochondrial genomes in human cells were investigated under different experimental conditions. Among mitochondrial transformants derived from an individual affected by the MERRF (myoclonus epilepsy associated with ragged red fibers) encephalomyopathy and carrying in heteroplasmic form the mitochondrial tRNALYS mutation associated with that syndrome, normal protein synthesis and respiration was observed when the wild-type mitochondrial DNA exceeded 10% of the total complement. In these transformants, the protective effect of wild-type mitochondrial DNA was shown to involve interactions of the mutant and wild-type gene products. Very different results were obtained in experiments in which two mitochondrial DNAs carrying nonallelic disease-causing mutations were sequentially introduced within distinct organelles into the same human mitochondrial DNA-less (p°) cell. In transformants exhibiting different ratios of the two genomes, no evidence of cooperation between their products was observed, even 3 months after the introduction of the second mutation. These results pointed to the phenotypic independence of the two genomes. A similar conclusion was reached in experiments in which mitochondria carrying a chloramphenicol resistance-inducing mitochondrial DNA mutation were introduced into chloramphenicol-sensitive cells. A plausible interpretation of the different results obtained in the latter two sets of experiments, compared with the complementation behavior observed in the heteroplasmic MERRF transformants, is that in the latter, the mutant and wild-type genomes coexisted in the same organelles from the time of the mutation. This would imply that the way in which mitochondrial DNA is sorted among different organelles plays a fundamental role in determining the oxidative-phosphorylation phenotype in mammalian cells. These results have significant implications for mitochondrial genetics and for studies on the transmission and therapy of mitochondrial DNA-linked diseases.Despite the large number of studies on the expression of artificially produced mitochondrial DNA (mtDNA) mutations and the phenotype of somatic cell hybrids and cybrids, information on mitochondrial genome interactions in mammalian cells is still very limited. The dependence of such interactions on the distribution of the mtDNA molecules among the mitochondria, which changes continuously throughout division and, possibly, fusion of the organelles, and the difficulty of investigating mtDNA sorting in a cell account in part for the present lack of understanding of how much the mitochondrial genomes interact in mammalian cells. The recent discovery of a variety of mtDNA mutations associated with diseases in humans (47) and the growing evidence of accumulation of mtDNA mutations with aging in somatic tissues (12-14, 19, 43) have raised a number of questions about the occurrence and frequency of intermixing of mutant and wild-type mtDNA and/or their products within a cell and the role that co...

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“…In CAP, this process was found to continue for up to 40 min. Thus, "in cells treated with antibiotics like CAP ribosomes continue to join to and move along mRNA in the absence of bulk protein synthesis" (28). These results suggest that for CAP and related inhibitors, lower drug concentrations might permit bacterial growth.…”

Section: Resultsmentioning

confidence: 97%

Assignment of two mitochondrially synthesized polypeptides to human mitochondrial DNA and their use in the study of intracellular mitochondrial interaction.

Oliver¹,

Wallace²

1982

Mol. Cell. Biol.

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Two mitochondrially synthesized marker polypeptides, MV-1 and MV-2, were found in human HeLa and HT1080 cells. These were assigned to the mitochondrial DNA in HeLa-HT1080 ybrids and hybrids by demonstrating their linkage to cytoplasmic genetic markers. These markers include mitochondrial DNA restriction site polymorphisms and resistance to chloramphenicol, an inhibitor of mitochondrial protein synthesis. In the absence of chloramphenicol, the expression of MV-1 and MV-2 in cybrids and hybrids was found to be directly proportional to the ratio of the parental mitochondrial DNAs. In the presence of chloramphenicol, the marker polypeptide linked to the chloramphenicol-sensitive mitochondrial DNA continued to be expressed. This demonstrated that resistant and sensitive mitochondrial DNAs can cooperate within a cell for gene expression and that the CAP-resistant allele was dominant or codominant to sensitive. Such cooperation suggests that mitochondrial DNAs can be exchanged between mitochondria.

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Polyribosome metabolism in Escherichia coli treated with chloramphenicol, neomycin, spectinomycin or tetracycline

Cited by 72 publications

References 29 publications

Recovery of Polysome Function of T4-Infected Escherichia coli After Brief Treatment with Chloramphenicol and Rifampin

Recovery of Polysome Function of T4-Infected Escherichia coli After Brief Treatment with Chloramphenicol and Rifampin

Complementation of mutant and wild-type human mitochondrial DNAs coexisting since the mutation event and lack of complementation of DNAs introduced separately into a cell within distinct organelles.

Assignment of two mitochondrially synthesized polypeptides to human mitochondrial DNA and their use in the study of intracellular mitochondrial interaction.

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