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Methicillin-resistant  Staphylococcus aureus  (MRSA) is intrinsically cross-resistant to virtually all β-lactam antibiotics. The central determinant for the MRSA phenotype is the  mecA  gene, whose transcriptional control may be mediated by a repressor ( mecI ) and a sensor/inducer ( mecR1 ). The  mecI-mecR1- mediated induction of  mecA  takes several hours rendering the strains phenotypically susceptible in spite of the presence of the resistance gene. Therefore, it has been proposed that the full resistance to β-lactams observed in many contemporary clinical MRSA strains requires a non-functional  mecI-mecR1  regulatory system. The  mecA  gene is embedded in a large chromosomal cassette (the SCC mec  element) for which several structural types have been described. Some epidemic MRSA clones, typically expressing full β-lactam resistance, carry SCC mec  elements that contain an intact  mecI-mecR1 locus  (e.g. SCC mec  types II and III). We have addressed this apparent contradiction by first sequencing the  mecI  coding region and  mecA  promoter sequences in a collection of prototype MRSA strains characterized by different SCC mec  types. A conserved non-sense mutation within  mecI  was detected in all SCC mec  type III strains tested, presumably responsible for a non-functional truncated MecI protein and, therefore, explaining the full resistance phenotype. In SCC mec  type II strains no conserved mutations were found. We next transformed a collection of prototype MRSA epidemic strains with a recombinant plasmid overexpressing a wild-type copy of  mecI . Surprisingly, for the great majority of the strains no significant alterations in the phenotypic expression of β-lactam resistance could be detected. These findings were confirmed and further explored, challenging the currently accepted mechanism of  mecA  transcriptional control. Our observations suggest the existence of yet unidentified additional determinants involved in the transcriptional control of  mecA  gene and point to a revision of the  mecA  regulatory mechanism in contemporary MRSA strains.

Methicillin-Resistance in Staphylococcus aureus Is Not Affected by the Overexpression in Trans of the mecA Gene Repressor: A Surprising Observation