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Staphylococcal species acquire antibiotic resistance by incorporating the mobile-genetic element SCC mec . We previously found that SCC mec -encoded  psm-mec  RNA suppresses exotoxin production as a regulatory RNA, and the  psm-mec  translation product increases biofilm formation in  Staphylococcus aureus . Here, we examined whether the regulatory role of  psm-mec  on host bacterial virulence properties is conserved among other staphylococcal species,  S. epidermidis  and  S. haemolyticus , both of which are important causes of nosocomial infections. In  S. epidermidis,  introduction of  psm-mec  decreased the production of cytolytic toxins called phenol-soluble modulins (PSMs) and increased biofilm formation.  Introduction  of  psm-mec  with a stop-codon mutation that did not express PSM-mec protein but did express  psm-mec  RNA also decreased PSM production, but did not increase biofilm formation. Thus, the  psm-mec  RNA inhibits PSM production, whereas the PSM-mec protein increases biofilm formation in  S. epidermidis.  In  S. haemolyticus,  introduction of  psm-mec  decreased PSM production, but did not affect biofilm formation. The mutated  psm-mec  with a stop-codon also caused the same effect. Thus, the  psm-mec  RNA also inhibits PSM production in  S. haemolyticus . These findings suggest that the inhibitory role of  psm-mec  RNA on exotoxin production is conserved among staphylococcal species, although the stimulating effect of the  psm-mec  gene on biofilm formation is not conserved.

Inhibition of Exotoxin Production by Mobile Genetic Element SCCmec-Encoded psm-mec RNA Is Conserved in Staphylococcal Species