Evidence for functional interaction between domains II and V of 23S ribosomal RNA from an erythromycin-resistant mutant.
A mutation affording low levels of erythromycin resistance has been obtained by in vitro hydroxylamine mutagenesis of a cloned ribosomal RNA operon from Escherichia coli. The site of the mutational event responsible for antibiotic resistance was localized to the gene region encoding domain II of 23S rRNA by replacement of restriction fragments in the wild-type plasmid by corresponding fragments from the mutant plasmid. DNA sequencing showed that positions 1219-1230 of the 23S rRNA gene are deleted in the mutant. Since all previously characterized rRNA mutations conferring resistance to erythromycin show changes exclusively in domain V, our present findings provide direct evidence for functional interaction between domains II and V of 23S rRNA.
D000667:Ampicillin / Q000494:pharmacology; D001483:Base Sequence; D002701:Chloramphenicol; D002874:Chromosome Mapping; D004917:Erythromycin / Q000494:pharmacology*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics; D009690:Nucleic Acid Conformation; D010403:Penicillin Resistance; D010957:Plasmids; D012335:RNA, Ribosomal / Q000235:genetics*
D012335:RNA, Ribosomal; D004917:Erythromycin; D002701:Chloramphenicol; D000667:Ampicillin