Role of mecA transcriptional regulation in the phenotypic expression of methicillin resistance in Staphylococcus aureus.

摘要: The gene required for methicillin resistance in staphylococci, mecA, encodes the low-affinity penicillin-binding protein 2a (PBP2a). Transcriptional regulation of mecA is accomplished some isolates by mecR1 and mecI, cotranscribed chromosomal genes that encode a putative signal transducer transcriptional repressor, respectively. Two Staphylococcus aureus strains have identical mecR1-mecI nucleotide sequences, BMS1 N315P, both exhibit low-level, heterotypic expression contain no beta-lactamase coregulatory sequences. was amplified from PCR shown to be functional on high-copy-number plasmid when introduced into an S. strain with deleted locus. Cloned repressed phenotypic resistance, transcription PBP2a production mediated induction response certain beta-lactam antibiotics. However, had different regulatory activities its native location N315P compared those BMS1. Uninduced markedly mecI inactivation increased 5- 40-fold, Furthermore, phenotype changed intact high-level, homotypic disrupted mecI. In contrast, uninduced produced abundant transcript PBP2a, while disruption effect little or production. Thus, mecI-mediated repression appears dysfunctional because presence absence additional cofactors. this independent regulation.