Relationships between bactericidal effect and inhibition of ribonucleic acid nucleotidyltransferase by rifampicin in Escherichia coli K-12.
The mechanism of action of rifampicin, an antibiotic which inhibits in vitro the polycondensation of ribonucleotides by ribonucleic acid (RNA) nucleotidyltransferase, was studied in vivo in Escherichia coli. It is argued that the inhibition of RNA nucleotidyltransferase represents the primary lesion and is responsible for the bactericidal effect. This conclusion is based on (i) the correlation between concentrations of the antibiotic which block in vivo incorporation of labeled uracil and the bactericidal concentrations, (ii) the evidence that the loss of viability of the cells immediately follows the block of RNA synthesis, and (iii) the observation that the reversal of the inhibition of RNA synthesis goes together with a reversal of the loss of viability.
D001426:Bacterial Proteins / Q000096:biosynthesis; D002247:Carbon Isotopes; D004269:DNA, Bacterial / Q000096:biosynthesis; D004926:Escherichia coli / Q000187:drug effects* / Q000378:metabolism; D010649:Phenylalanine / Q000378:metabolism; D012316:RNA Nucleotidyltransferases / Q000037:antagonists & inhibitors*; D012329:RNA, Bacterial / Q000096:biosynthesis; D012293:Rifampin / Q000494:pharmacology*; D013941:Thymine / Q000378:metabolism; D014498:Uracil / Q000378:metabolism
D001426:Bacterial Proteins; D002247:Carbon Isotopes; D004269:DNA, Bacterial; D012329:RNA, Bacterial; D010649:Phenylalanine; D014498:Uracil; D012316:RNA Nucleotidyltransferases; D013941:Thymine; D012293:Rifampin