Member of the two-component regulatory system VraS/VraR involved in the control of the cell wall peptidoglycan biosynthesis. Upon cellular stress, the histidine kinase VraS transfers the phosphoryl group onto VraR. Upon phosphorylation, VraR dimerizes at the N-terminal domain. In turn, phosphorylation-induced dimerization expands and enhances the VraR binding to its own promoter leading to increased expression and subsequent modulation of as many as 40 genes, which ultimately constitute the S.aureus response to cell wall damage (By similarity). In addition, inhibits the host autophagic flux and delays the early stage of autophagosome formation, thereby promoting bacterial survival. Facilitates the ability of S.aureus to resist host polymorphonuclear leukocytes-mediated phagocytosis and killing thus contributing to immune evasion (By similarity). Homodimer. Phosphorylated by VraS. Phosphorylation state of VraR controls dimerization of the protein.