| SaeRS |
β-Lactam antibiotics
or human neutrophil peptides |
Implicated in the expression
of 212 genes. Up-regulation results in increased expression of many
virulence factors including cell wall proteins, cell-wall-associated
proteins, and secreted proteins. |
(21, 22) |
| ArlRS |
Undetermined |
Implicated to control the
expression of 114 genes. Activation leads to down-regulation of transcription
of some virulence genes (α-toxin, β-hemolysin, lipase,
serine protease, coagulase, and protein A). Also plays a key role in autolysis which is essential in bacterial
cell division and can be triggered by antibiotics or adverse physiological
conditions. |
(23, 24) |
| SrrAB |
Reduced oxygen levels;
however,
other factors that reflect the oxygen level or redox state such as
pH may act as the signal. |
Up-regulation increases
expression of colonization factors and a number of proteins involved
in energy metabolism. Repression results in the up-regulation of virulence
factors including TSST-1and RNAIII. |
(25) |
| KdpDE |
Autoinducer-2 (AI-2) and
external K+ levels |
High extracellular K+ levels result in reduced KdpDE expression resulting in increased
expression extracellular toxins and enzymes. Reduced K+ levels activate KdpDE transcription, increasing the expression of
cell wall proteins and polysaccharides, which are beneficial to colonization. |
(26, 27) |
| AgrCA |
Autoinducing peptides (AIPs) |
Regulation of numerous metabolic,
virulence, and regulatory genes through RNAIII dependent and independent
mechanisms |
(17, 18) |
| LytRS |
Postulated to be triggered
by anaerobic metabolism |
Inhibits the extracellular
activity of murein hydrolases. These enzymes catalyze the cleavage
of specific structural components of the bacterial cell wall, aiding
penicillin tolerance. Additionally activated LytR is hypothesized
to induce lrgAB promoter activity which promotes cell death and lysis
during biofilm development. |
(30) |
| VraRS |
Possible activators include
glycopeptide antibiotics, e.g., vancomycin and teicoplanin. |
VraRS system regulates a
response to cell wall stress. Inactivation results in reduced cell
wall thickness an increase susceptibility to glycopeptide antibiotics. |
(31, 32) |
| GraRS |
Low external salt concentrations |
Activation positively regulates
expression of the dlt operon. This operon encodes
proteins responsible for d-alanylation. Addition of d-alanine to teichoic acids reduces the negative charge of the cell
envelope, thereby influencing the binding and interaction of various
compounds. d-Alanylation helps to protect from antimicrobial
peptides. |
(33) |
