The ability to form robust biofilms and secrete a diverse array of virulence factors are key pathogenic determinants of , causing a wide range of infectious diseases. Here, we characterized as a VraR-regulated gene encoding a cell wall inhibition-responsive protein (CwrA) using electrophoretic mobility shift assays. We constructed deletion mutants in the genetic background of methicillin-resistant (MRSA) and methicillin-sensitive (MSSA) strains. Phenotypic analyses indicated that deletion of led to impaired biofilm formation, which was correlated with polysaccharide intercellular adhesin (PIA). Besides, the results of real-time quantitative PCR (RT-qPCR) and β-galactosidase activity assay revealed that CwrA promoted biofilm formation by influence the operon activity in . Furthermore, deletion mutants released less extracellular DNA (eDNA) in the biofilm because of their reduced autolytic activity compared to the wild-type (WT) strains. We also found that deletion mutant more virulence than the parental strain because of its enhanced hemolytic activity. Mechanistically, this phenotypic alteration is related to activation of the SaeRS two-component system, which positively regulates the transcriptional levels of genes encoding membrane-damaging toxins. Overall, our results suggest that CwrA plays an important role in modulating biofilm formation and hemolytic activity in .
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457683 | PMC |
http://dx.doi.org/10.1080/21505594.2024.2411540 | DOI Listing |
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