The SaeRS Two‐Component System of Staphylococcus aureus

Abstract

In the Gram-positive pathogenic bacterium Staphylococcus aureus, the SaeRS two-component system (TCS) plays a major role in controlling the production of over 20 virulence factors including hemolysins, leukocidins, superantigens, surface proteins, and proteases. The SaeRS TCS is composed of the sensor histidine kinase SaeS, response regulator SaeR, and two auxiliary proteins SaeP and SaeQ. Since its discovery in 1994, the sae locus has been studied extensively, and its contributions to staphylococcal virulence and pathogenesis have been well documented and understood; however, the molecular mechanism by which the SaeRS TCS receives and processes cognate signals is not. In this article, therefore, we review the literature focusing on the signaling mechanism and its interaction with other global regulators.

Revisiting the regulation of the capsular polysaccharide biosynthesis gene cluster in Staphylococcus aureus

“…While Sae, CodY and Rot all interfered with SigB‐dependent promoter activity, only Sae additionally repressed activity of the SigA‐dependent promoter. This is in line with a predicted SaeR binding site located between the two promoters (Liu et al , ). We hypothesize that the repression of SigB‐dependent promoter activity occurs via steric interference, whereas the SigA‐dependent promoter activity might be repressed via a roadblock mechanism.…”

“…5B). Binding is consistent with a putative SaeR binding motif located between −79 bp and −94 bp upstreams of the capA start codon (Liu et al, 2016). Specific binding to the P cap upstream region was also found for Rot and CodY ( Fig.…”

Rational Design of Selective Adenine-Based Scaffolds for Inactivation of Bacterial Histidine Kinases

“…8 For example, in the pathogenic bacterium Staphylococcus aureus , the SaeRS TCS affects the production of over 20 virulence factors. 9 The PhoPR system controls polyketide-derived lipid biosynthesis in Mycobacterium tuberculosis , and its absence causes dramatic changes to colonial and cording morphology of this highly dangerous microbe. 10 In Pseudomonas aeruginosa , many TCSs, including PPrBA, are responsible for activating virulence genes, cell motility, and quorum sensing signal production.…”

Fisiopatología de la sepsis por gram positivos

“…El Staphylococcus aureus es capaz de secretar entre 23 a 24 superantígenos diferentes serológicamente dentro de los que se encuentran más de 20 enterotoxinas estafi lococcicas (SEs del inglés) entre estas la TSST-1, las SEs con serotipos A, B n , C n , (N=múltiples variantes) D, E, F y G; y la SE -1 (serotipo H, I y J a la X). En función de muchos de estos superantígenos, especialmente el SEA, y con menos frecuencia el SEG, SEC, SEI, se ha explicado la patogénesis de los S.aureus y su evolución hacia la sepsis; así como la patogénesis de los S.aureus meticilina resistentes (MRSA en inglés) asociados a sepsis letal, endocarditis infecciosa y lesión renal en modelos animales debido específi camente a sus superantígenos SEA y SEC, así como al gen mecA que codifi ca la proteína de unión a la penicilina alterada (PBP2a) que es su principal mecanismo de resistencia a la meticilina lo que les hace unos de los microorganismos que más centran la atención en los últimos años de la comunidad científi ca y médica al ser responsables del aumento de la tasas de morbilidad y mortalidad de infecciones por estafi lococos a nivel hospitalario y comunitario dada la multirresistencia que exhiben y el estar asociados (19)(20)(21)(22)(23)(24)(25)(26)(27).…”