Analysis of a kanamycin resistance gene(kmr) fromStreptomyces kanamyceticus and a mutant with increased aminoglycoside resistance

Demydchuk, Julia; Oliynyk, Zoryana; Fedorenko, Victor

doi:10.1002/(sici)1521-4028(199809)38:4<231::aid-jobm231>3.0.co;2-w

Cited by 13 publications

(4 citation statements)

References 10 publications

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“…Identities with other 16S rRNA methylases produced by Streptomyces and Micromonospora species were generally lower. Amino acid identities of RmtB were 33 and 32% with GrmB and Sgm methylases of sisomicin-producing Micromonospora rosea and Micromonospora zionensis, respectively (14); 32% with GrmA methylase of gentamicin-producing Micromonospora purpurea (14); 31% with Kmr methylase of kanamycin-producing Streptomyces kanamyceticus (8); 30% with FmrO methylase of fortimicin-producing Micromonospora olivasterospora (18); and 27% with KgmB of nebramycin-producing Streptomyces tenebrarius (12). The putative promoter region of rmtB appeared to be located within the right-hand end of Tn3, just upstream of the inverted repeat (Fig.…”

Section: Resultsmentioning

confidence: 99%

Plasmid-Mediated 16S rRNA Methylase in Serratia marcescens Conferring High-Level Resistance to Aminoglycosides

Doi

Yokoyama

Yamane

et al. 2004

Antimicrob Agents Chemother

170

118

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Serratia marcescens S-95, which displayed an unusually high degree of resistance to aminoglycosides, including kanamycins and gentamicins, was isolated in 2002 from a patient in Japan. The resistance was mediated by a large plasmid which was nonconjugative but transferable to an Escherichia coli recipient by transformation. The gene responsible for the aminoglycoside resistance was cloned and sequenced. The deduced amino acid sequence of the resistance gene shared 82% identity with RmtA, which was recently identified as 16S rRNA methylase conferring high-level aminoglycoside resistance in Pseudomonas aeruginosa. Histidine-tagged recombinant protein showed methylation activity against E. coli 16S rRNA. The novel aminoglycoside resistance gene was therefore designated rmtB. The genetic environment of rmtB was further investigated. The sequence immediately upstream of rmtB contained the right end of transposon Tn3, including bla TEM , while an open reading frame possibly encoding a transposase was identified downstream of the gene. This is the first report describing 16S rRNA methylase production in S. marcescens. The aminoglycoside resistance mechanism mediated by production of 16S rRNA methylase and subsequent ribosomal protection used to be confined to aminoglycoside-producing actinomycetes. However, it is now identified among pathogenic bacteria, including Enterobacteriaceae and P. aeruginosa in Japan. This is a cause for concern since other treatment options are often limited in patients requiring highly potent aminoglycosides such as amikacin and tobramycin.

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Section: Resultsmentioning

confidence: 99%

Plasmid-Mediated 16S rRNA Methylase in Serratia marcescens Conferring High-Level Resistance to Aminoglycosides

Doi

Yokoyama

Yamane

et al. 2004

Antimicrob Agents Chemother

170

118

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“…The MICs of the antibiotics were determined by agar dilution with ca. 10 4 CFU per spot after 18 h of incubation at 37°C.…”

Section: Methodsmentioning

confidence: 99%

Plasmid-Mediated High-Level Resistance to Aminoglycosides in Enterobacteriaceae Due to 16S rRNA Methylation

Galimand

Courvalin

Lambert

2003

Antimicrob Agents Chemother

321

221

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A self-transferable plasmid of ca. 80 kb, pIP1204, conferred multiple-antibiotic resistance to Klebsiella pneumoniae BM4536, which was isolated from a urinary tract infection. Resistance to ␤-lactams was due to the bla TEM1 and bla CTX-M genes, resistance to trimethroprim was due to the dhfrXII gene, resistance to sulfonamides was due to the sul1 gene, resistance to streptomycin-spectinomycin was due to the ant3؆9 gene, and resistance to nearly all remaining aminoglycosides was due to the aac3-II gene and a new gene designated armA (aminoglycoside resistance methylase). The cloning of armA into a plasmid in Escherichia coli conferred to the new host high-level resistance to 4,6-disubstituted deoxystreptamines and fortimicin. The deduced sequence of ArmA displayed from 37 to 47% similarity to those of 16S rRNA m 7 G methyltransferases from various actinomycetes, which confer resistance to aminoglycoside-producing strains. However, the low guanine-pluscytosine content of armA (30%) does not favor an actinomycete origin for the gene. It therefore appears that posttranscriptional modification of 16S rRNA can confer high-level broad-range resistance to aminoglycosides in gram-negative human pathogens.

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“…87 A number of genes encoding such enzymes have been identified from several aminoglycoside producers. [88][89][90][91][92][93][94][95] The corresponding rRNA methyltransferases form the Agr family of methyltransferases (for aminoglycoside resistance). 96 Some of these enzymes have been characterized.…”

Section: S Rrna Methylationmentioning

confidence: 99%

Molecular Insights into Aminoglycoside Action and Resistance

2004

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Analysis of a kanamycin resistance gene(kmr) fromStreptomyces kanamyceticus and a mutant with increased aminoglycoside resistance

Cited by 13 publications

References 10 publications

Plasmid-Mediated 16S rRNA Methylase in Serratia marcescens Conferring High-Level Resistance to Aminoglycosides

Plasmid-Mediated 16S rRNA Methylase in Serratia marcescens Conferring High-Level Resistance to Aminoglycosides

Plasmid-Mediated High-Level Resistance to Aminoglycosides in Enterobacteriaceae Due to 16S rRNA Methylation

Molecular Insights into Aminoglycoside Action and Resistance

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