Staphylococci are common commensals in human beings, yet certain species are pathogenic. Staphylococcus aureus, particularly, is a very virulent human pathogen. The capacity of staphylococci to sense the density of bacterial cell, i.e., quorum, and thereafter respond via genetic modifications is attributable to one primary mechanism known as accessory gene regulator (Agr). Agr's extracellular signal is a peptide that is posttranslationally modified with a thiolactone molecule. Agr is in charge of the upregulation of numerous exotoxins and hydrolyzing enzymes, as well as the downregulation of many colonization determinants, under circumstances of high cell density. This modulation is critical for the scheduling synthesis of virulence determinants throughout the infection course and the establishment of acute illness, whereas low Agr activity is linked to persistent staphylococcal infections, such as biofilm development. Moreover, Staphylococcal Accessory Regulator Aِ (SarA) controls the establishment of biofilm in S. aureus that hinders the production of nuclease and protease via triggering the P2 and P3 promoters resulting in the activation of RNAII and RNAIII, respectively. SarA also endures the transcription of agrA and saeS, and many virulence determinants including hla, hlb, and hlg coding α-, β-, and γ-hemolysins, respectively. Upon the aforementioned facts, the present review will shed some light on the Quorum Sensing (QS) in S. aureus, particularly, the Agr and Sar systems and how these systems control the pathogenicity of this spe
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