1995
DOI: 10.1128/jb.177.15.4327-4332.1995
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Substrate requirements for ErmC' methyltransferase activity

Abstract: ErmC is a methyltransferase that confers resistance to the macrolide-lincosamide-streptogramin B group of antibiotics by catalyzing the methylation of 23S rRNA at a specific adenine residue (A-2085 in Bacillus subtilis; A-2058 in Escherichia coli). The gene for ErmC was cloned and expressed to a high level in E. coli, and the protein was purified to virtual homogeneity. Studies of substrate requirements of ErmC have shown that a 262-nucleotide RNA fragment within domain V of B. subtilis 23S rRNA can be utilize… Show more

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Cited by 31 publications
(16 citation statements)
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“…1a). In contrast to various domain V constructs used in previous studies (6)(7)(8)19), which contained extra nucleotides before the 5= end of helix 73 and/or after its 3= end, domain V harboring only the exact helix 73 was used in this study, from which gradual truncation was performed to define the end nucleotide or base pair for accepting the methyl group from S-adenosyl-L-methionine (SAM) with the action of Erm proteins (Fig. 1a).…”
Section: Resultsmentioning
confidence: 99%
“…1a). In contrast to various domain V constructs used in previous studies (6)(7)(8)19), which contained extra nucleotides before the 5= end of helix 73 and/or after its 3= end, domain V harboring only the exact helix 73 was used in this study, from which gradual truncation was performed to define the end nucleotide or base pair for accepting the methyl group from S-adenosyl-L-methionine (SAM) with the action of Erm proteins (Fig. 1a).…”
Section: Resultsmentioning
confidence: 99%
“…Due to methylation, the minimal inhibitory concentrations required to inhibit bacterial growth increase from 2 to 512 μ g/ml for clindamycin and from 16 to 8000 μ g/ml for lincomycin. Bacteria resistant to lincosamides also exhibit resistance to macrolides [ 11 13 ] with a similar mechanism, i.e., due to modifications of A2058. In addition to bacterial resistance, lincosamides also have side effects such as diarrhea, nausea, rash, hypersensitivity, and jaundice [ 14 , 15 ], which further limit their efficiency in therapy.…”
Section: Introductionmentioning
confidence: 99%
“…Ketolides have largely addressed resistance due to drug efflux and metabolism yet still remain susceptible to ribosomal modification [13], [14], the most clinically relevant of which is modification of A2058 in 23S rRNA ( E. coli numbering throughout) that confers cross-resistance to antibiotics in the macrolide, lincosamide and streptogramin B classes (MLS) [15][18]. A2058-based resistance includes mutation of A2058 to G as well as methylation of the exocyclic N6 of A2058 via the expression of erm genes encoding methyltransferases (Erm methyltransferases) that add one or two methyl groups and represent the most effective mechanism of macrolide resistance [19]–[21]. Telithromycin and other ketolides have been found to mitigate macrolide resistance due to the A2058G mutation ( Table S1 in Text S1 ) [22][24], though ketolides that are widely effective against Erm methylation-based modifications are not known.…”
Section: Introductionmentioning
confidence: 99%