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CovR/CovS is an important two-component regulatory system in human pathogen group A  Streptococcus  (GAS). Epidemiological studies have shown that inactivation of the sensor kinase CovS is correlated with invasive clinical manifestations. The phosphorylation level of response regulator CovR decreases dramatically in the absence of CovS, resulting in the derepression of virulence factor expression and an increase in bacterial invasiveness. Streptococcal pyrogenic exotoxin B (SpeB) is a cysteine protease and is negatively regulated by CovR; however, the expression of SpeB is almost completely repressed in the  covS  mutant. The present study found that in the  emm1- type A20 strain, non-phosphorylated CovR acts as a transcriptional repressor for SpeB-positive regulator Rgg. In addition, the expression of Rgg-negative regulator LacD.1 is upregulated in the  covS  mutant. These results suggest that inactivation of Rgg in the  covS  mutant would directly mediate  speB  repression. The current study showed that overexpression of  rgg  but not inactivation of  lacD.1  in the  covS  mutant partially restores  speB  expression, indicating that only  rgg  repression, but not  lacD.1  upregulation, contributes to the  speB  repression in the  covS  mutant.

Repression of Rgg But Not Upregulation of LacD.1 in emm1-type covS Mutant Mediates the SpeB Repression in Group A Streptococcus