title: Inhibition of exotoxin production by mobile genetic element SCCmec-encoded psm-mec RNA is conserved in staphylococcal species.
abstract: Staphylococcal species acquire antibiotic resistance by incorporating the mobile-genetic element SCCmec. We previously found that SCCmec-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.
authors.affiliation: Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Mariko
authors.initials: M
authors.lastname: Ikuo
authors.affiliation: Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Gentaro
authors.initials: G
authors.lastname: Nagano
authors.affiliation: Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Yuki
authors.initials: Y
authors.lastname: Saito
authors.affiliation: Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Han
authors.initials: H
authors.lastname: Mao
authors.affiliation: Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Sekimizu
authors.affiliation: Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: Chikara
authors.initials: C
authors.lastname: Kaito
mesh_terms: D018441:Biofilms / Q000254:growth & development; D017124:Conserved Sequence; D005098:Exotoxins / Q000235:genetics*; D015964:Gene Expression Regulation, Bacterial; D020868:Gene Silencing / Q000502:physiology*; D020071:Interspersed Repetitive Sequences / Q000502:physiology*; D010641:Phenotype; D012329:RNA, Bacterial / Q000235:genetics*; D013210:Staphylococcus / Q000235:genetics* / Q000254:growth & development / Q000472:pathogenicity; D013211:Staphylococcus aureus / Q000235:genetics / Q000254:growth & development; D013212:Staphylococcus epidermidis / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity; D041162:Staphylococcus haemolyticus / Q000235:genetics / Q000254:growth & development / Q000472:pathogenicity; D014774:Virulence / Q000235:genetics
chemical_list: D005098:Exotoxins; D012329:RNA, Bacterial