Construction and characterization of ∆vraSR-lrgAB of Staphylococcus epidermidis

Abstract:

Objective To explore the role of VraSR in regulating the biological functions of Staphylococcus epidermidis via the CidA-LrgAB system.Methods The recombinant plasmid pKOR1-ΔlrgAB was constructed and then electroporated into SE1457 ?vraSR to delete lrgAB from the genome of ?vraSR by homologous recombination. The suspected mutant ?vraSR-lrgAB was verified by PCR, RT-PCR, and sequencing. The growth, drug susceptibility, autolysis, and biofilm formation of ?vraSR-lrgAB were determined.Results The S. epidermidis mutant ?vraSR-lrgAB was successfully constructed. Compared with SE1457, ?vraSR, and ?lrgAB, ?vraSR-lrgAB exhibited retarded growth, especially at 25 ℃ and 40 ℃ (P<0.001), increased drug susceptibility (P<0.01), enhanced autolysis (P<0.001), and reduced biofilm formation (P<0.01).Conclusion VraSR may regulate the growth, drug susceptibility, autolysis, and biofilm formation of S. epidermidis partly via the LrgAB system.