Structural highlights
Function
ARLR_STAA8 Member of the two-component regulatory system ArlS/ArlR involved in the regulation of adhesion, autolysis, multidrug resistance and virulence. ArlS/ArlR affects expression of the multidrug resistance transporter NorA and interacts with both Agr (virulence accessory gene regulator) (negatively) and SarA (staphylococcal accessory regulator) (positively) to modulate several virulence factor genes, including ssp (serine protease), spa (surface protein A) and hla (alpha-hemolysin). Could inhibit biofilm development by a mechanism independent of the presence of the poly-N-acetylglucosamine (PNAG). Also, Arl proteins are required for the efficient activity of DNA gyrase inhibitors and high osmolarity on spa expression.[1] [2] [3] [4] [5]
See Also
References
- ↑ Fournier B, Aras R, Hooper DC. Expression of the multidrug resistance transporter NorA from Staphylococcus aureus is modified by a two-component regulatory system. J Bacteriol. 2000 Feb;182(3):664-71. PMID:10633099 doi:10.1128/JB.182.3.664-671.2000
- ↑ Fournier B, Hooper DC. A new two-component regulatory system involved in adhesion, autolysis, and extracellular proteolytic activity of Staphylococcus aureus. J Bacteriol. 2000 Jul;182(14):3955-64. PMID:10869073 doi:10.1128/JB.182.14.3955-3964.2000
- ↑ Fournier B, Klier A, Rapoport G. The two-component system ArlS-ArlR is a regulator of virulence gene expression in Staphylococcus aureus. Mol Microbiol. 2001 Jul;41(1):247-61. PMID:11454217 doi:10.1046/j.1365-2958.2001.02515.x
- ↑ Fournier B, Klier A. Protein A gene expression is regulated by DNA supercoiling which is modified by the ArlS-ArlR two-component system of Staphylococcus aureus. Microbiology (Reading). 2004 Nov;150(Pt 11):3807-3819. PMID:15528666 doi:10.1099/mic.0.27194-0
- ↑ Toledo-Arana A, Merino N, Vergara-Irigaray M, Débarbouillé M, Penadés JR, Lasa I. Staphylococcus aureus develops an alternative, ica-independent biofilm in the absence of the arlRS two-component system. J Bacteriol. 2005 Aug;187(15):5318-29. PMID:16030226 doi:10.1128/JB.187.15.5318-5329.2005
