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Replicating methicillin resistance?

Nature Structural & Molecular Biology volume 23, pages 874–875 (2016)Cite this article

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Methicillin resistance in the clinically important bacterium Staphylococcus aureus (MRSA) has evolved in multiple S. aureus lineages through acquisition of chromosomally integrating mobile genetic elements named SCCmec. Now Rice and colleagues show that the conserved SCCmec cch gene encodes an active DNA helicase, thus suggesting that extrachromosomal replication is part of the enigmatic SCCmec horizontal-transfer mechanism.

Large chromosomally integrating mobile genetic elements, or genomic islands, are widespread in bacteria and confer diverse traits involved in pathogenicity, antimicrobial resistance, symbiosis and metabolism. Genomic islands are usually flanked by a short direct-repeat DNA sequence that delineates the element-insertion site within the chromosome. Recombination of the direct-repeat sequences, through the action of site-specific recombinases, results in the excision and formation of a circularized element that acts as the DNA substrate for horizontal transfer5. After excision, integrative and conjugative elements (ICEs) can transfer to other bacteria through conjugation, whereas some pathogenicity islands, such as S. aureus SAPI, are packaged into bacteriophage capsids after phage infection. Like other genomic islands, SCCmec elements have been demonstrated to excise and circularize3,6, but further information relating to the mechanism of horizontal transfer is scant. Attempts to transfer SCCmec elements through phage transduction7,8 or conjugative mobilization9 have been met with varying degrees of success, and it remains uncertain whether the mechanisms demonstrated are used by SCCmec during natural transfer.

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Figure 1: Conserved genetic organization of SCCmec.

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  1. Joshua P. Ramsay is at the School of Biomedical Sciences and the Curtin Health Innovation Research Institute, Curtin University, Perth, Australia.,

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Ramsay, J. Replicating methicillin resistance?. Nat Struct Mol Biol 23, 874–875 (2016). https://doi.org/10.1038/nsmb.3303

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