A non-coding RNA from the intercellular adhesion (ica) locus of Staphylococcus epidermidis controls polysaccharide intercellular adhesion (PIA)-mediated biofilm formation.

Abstract

Polysaccharide intercellular adhesin (PIA)-associated biofilm formation is mediated by the intercellular adhesin (ica) locus and represents a major pathomechanism of Staphylococcus epidermidis. Here, we report on a novel long non-coding (nc)RNA, named IcaZ, which is approximately 400 nucleotides in size. icaZ is located downstream of the ica repressor gene icaR and partially overlaps with the icaR 3' UTR. icaZ exclusively exists in ica-positive S. epidermidis, but not in S. aureus or other staphylococci. Inactivation of the gene completely abolishes PIA production. IcaZ is transcribed as a primary transcript from its own promoter during early- and mid-exponential growth and its transcription is induced by low temperature, ethanol and salt stress. IcaZ targets the icaR 5' UTR and hampers icaR mRNA translation, which alleviates repression of icaADBC operon transcription and results in PIA production. Interestingly, other than in S. aureus, posttranscriptional control of icaR mRNA in S. epidermidis does not involve icaR mRNA 5'/3' UTR base pairing. This suggests major structural and functional differences in icaADBC operon regulation between the two species that also involve the recruitment of ncRNAs. Together, the IcaZ ncRNA represents an unprecedented novel species-specific player involved in the control of PIA production in NBSP S. epidermidis.