Tandem duplication in ermC translational attenuator of the macrolide-lincosamide-streptogramin B resistance plasmid pSES6 from Staphylococcus equorum | Zendy

Gabriele Lodder | Zendy; Štefan Schwarz | Zendy; Philip D. Gregory | Zendy; K. G. H. Dyke | Zendy

Open Access

Tandem duplication in ermC translational attenuator of the macrolide-lincosamide-streptogramin B resistance plasmid pSES6 from Staphylococcus equorum

Author(s) -

Gabriele Lodder,

Štefan Schwarz,

Philip D. Gregory,

K. G. H. Dyke

Publication year - 1996

Publication title -

antimicrobial agents and chemotherapy

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.07

H-Index - 259

eISSN - 1070-6283

pISSN - 0066-4804

DOI - 10.1128/aac.40.1.215

Subject(s) - ribosomal binding site , biology , ribosome , plasmid , attenuator (electronics) , gene duplication , gene , tandem exon duplication , genetics , 23s ribosomal rna , coding region , microbiology and biotechnology , rna , physics , attenuation , optics

A tandem duplication of 23 bp in the ermC gene translational attenuator of plasmid pSES6 from Staphylococcus equorum which mediated constitutive resistance to macrolide-lincosamide-streptogramin B antibiotics was identified. This duplication included the ribosome binding site for the ermC gene as well as the first 5 bp of the ermC coding sequence. It was postulated that this sequence duplication affects the possible RNA conformations so that the ribosome binding site for ErmC synthesis is readily accessible to the ribosomes and thus constitutive expression of the ermC gene occurs.

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