The pathogenesis of Staphylococcus aureus, from local infections
to systemic dissemination, is mediated by a battery
of virulence factors that are regulated by intricate mechanisms,
which include regulatory proteins and small RNAs
(sRNAs) as key regulatory molecules. We have investigated
the involvement of sRNA RsaF, in the regulation of pathogenicity
genes hyaluronate lyase (hysA) and serine proteaselike
protein D (splD), by employing S. aureus strains with disruption
and overexpression of rsaF. Staphylococcus aureus
strain with disruption of rsaF exhibited marked down-regulation
of hysA transcripts by 0.2 to 0.0002 fold, and hyaluronate
lyase activity by 0.2–0.1 fold, as well as increased biofilm
formation, during growth from log phase to stationery
phase. These mutants also displayed down-regulation of splD
transcripts by 0.8 to 0.005 fold, and reduced activity of multiple
proteases by zymography. Conversely, overexpression of
rsaF resulted in a 2- to 4- fold increase in hysA mRNA levels
and hyaluronidase activity. Both hysA and splD mRNAs demonstrated
an increased stability in RsaF+ strains. In silico
RNA-RNA interaction indicated a direct base pairing of RsaF
with hysA and splD mRNAs, which was established in electrophoretic
mobility shift assays. The findings demonstrate
a positive regulatory role for small RNA RsaF in the expression
of the virulence factors, HysA and SplD.
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