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Group B streptococcal haemolysin and pigment, a tale of twins.

Rosa-Fraile M, Dramsi S, Spellerberg B - FEMS Microbiol. Rev. (2014)

Bottom Line: However, the biochemical nature of the GBS haemolysin has remained elusive for almost a century because of its instability during purification procedures.Recently, it has been suggested that the haemolytic and cytolytic activity of GBS is due to the ornithine rhamnopolyenic pigment and not to the CylE protein.Here we review and summarize our current knowledge of the genetics, regulation and biochemistry of these twin GBS phenotypic traits, including their functions as GBS virulence factors.

View Article: PubMed Central - PubMed

Affiliation: Service of Microbiology, Hospital Virgen de las Nieves, Granada, Spain.

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Related in: MedlinePlus

Regulators controlling transcription of the cyl operon. The two-component system CovS/R represents the major regulator of haemolysis and pigmentation in GBS. In wild-type strains the response regulator CovR is phosphorylated through CovS and bound to the cyl promotor region. Binding of CovR results in a repression of cyl gene transcription. This repression is modulated by an inhibition of CovR through the serine threonine kinase Skt1 and an inhibition of CovS through the Abi domain protein Abx1. In addition, the RovS regulator as a stand-alone system can increase haemolysin and pigment expression through binding to the cyl promotor region.
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fig03: Regulators controlling transcription of the cyl operon. The two-component system CovS/R represents the major regulator of haemolysis and pigmentation in GBS. In wild-type strains the response regulator CovR is phosphorylated through CovS and bound to the cyl promotor region. Binding of CovR results in a repression of cyl gene transcription. This repression is modulated by an inhibition of CovR through the serine threonine kinase Skt1 and an inhibition of CovS through the Abi domain protein Abx1. In addition, the RovS regulator as a stand-alone system can increase haemolysin and pigment expression through binding to the cyl promotor region.

Mentions: Additional regulatory elements were shown to allow the fine-tuning of CovS/R and therefore indirectly control β-haemolysin expression. GBS encodes a single eukaryotic-type membrane-associated serine/threonine kinase Stk1 and its cognate, soluble protein, serine/threonine phosphatase Stp1 (Rajagopal et al., 2003; Burnside et al., 2011). Stp1 phosphorylates CovR on threonine 65, which decreases the phosphorylation of CovR at Asp53 relieving the CovR-mediated repression of the cyl operon. Stk1 positively regulates transcription of β-h/c, which is critical for GBS virulence, and Stk1 mutants produce less β-h/c compared with wild-type strains (Rajagopal et al., 2006; Lin et al., 2009). Stp1 is the cognate phosphatase of Stk1, and indeed Stp1 mutants exhibit several phenotypes such as decreased haemolytic activity, increased autolysis and a reduction in the ability to cause systemic infections (Burnside et al., 2011). Abx1 was recently identified as the third partner of the CovS/R system in GBS through direct interaction with CovS (Firon et al., 2013). RovS, a stand-alone transcriptional regulator, activates the expression of cylE and other genes of the cyl operon through direct binding to the promoter region (Samen et al., 2006). Thus, multiple signals sensed through CovS, Stk1 and Abx1 are integrated via CovS/R to fine-tune haemolysin expression (Firon et al., 2013; Fig. 3).


Group B streptococcal haemolysin and pigment, a tale of twins.

Rosa-Fraile M, Dramsi S, Spellerberg B - FEMS Microbiol. Rev. (2014)

Regulators controlling transcription of the cyl operon. The two-component system CovS/R represents the major regulator of haemolysis and pigmentation in GBS. In wild-type strains the response regulator CovR is phosphorylated through CovS and bound to the cyl promotor region. Binding of CovR results in a repression of cyl gene transcription. This repression is modulated by an inhibition of CovR through the serine threonine kinase Skt1 and an inhibition of CovS through the Abi domain protein Abx1. In addition, the RovS regulator as a stand-alone system can increase haemolysin and pigment expression through binding to the cyl promotor region.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4315905&req=5

fig03: Regulators controlling transcription of the cyl operon. The two-component system CovS/R represents the major regulator of haemolysis and pigmentation in GBS. In wild-type strains the response regulator CovR is phosphorylated through CovS and bound to the cyl promotor region. Binding of CovR results in a repression of cyl gene transcription. This repression is modulated by an inhibition of CovR through the serine threonine kinase Skt1 and an inhibition of CovS through the Abi domain protein Abx1. In addition, the RovS regulator as a stand-alone system can increase haemolysin and pigment expression through binding to the cyl promotor region.
Mentions: Additional regulatory elements were shown to allow the fine-tuning of CovS/R and therefore indirectly control β-haemolysin expression. GBS encodes a single eukaryotic-type membrane-associated serine/threonine kinase Stk1 and its cognate, soluble protein, serine/threonine phosphatase Stp1 (Rajagopal et al., 2003; Burnside et al., 2011). Stp1 phosphorylates CovR on threonine 65, which decreases the phosphorylation of CovR at Asp53 relieving the CovR-mediated repression of the cyl operon. Stk1 positively regulates transcription of β-h/c, which is critical for GBS virulence, and Stk1 mutants produce less β-h/c compared with wild-type strains (Rajagopal et al., 2006; Lin et al., 2009). Stp1 is the cognate phosphatase of Stk1, and indeed Stp1 mutants exhibit several phenotypes such as decreased haemolytic activity, increased autolysis and a reduction in the ability to cause systemic infections (Burnside et al., 2011). Abx1 was recently identified as the third partner of the CovS/R system in GBS through direct interaction with CovS (Firon et al., 2013). RovS, a stand-alone transcriptional regulator, activates the expression of cylE and other genes of the cyl operon through direct binding to the promoter region (Samen et al., 2006). Thus, multiple signals sensed through CovS, Stk1 and Abx1 are integrated via CovS/R to fine-tune haemolysin expression (Firon et al., 2013; Fig. 3).

Bottom Line: However, the biochemical nature of the GBS haemolysin has remained elusive for almost a century because of its instability during purification procedures.Recently, it has been suggested that the haemolytic and cytolytic activity of GBS is due to the ornithine rhamnopolyenic pigment and not to the CylE protein.Here we review and summarize our current knowledge of the genetics, regulation and biochemistry of these twin GBS phenotypic traits, including their functions as GBS virulence factors.

View Article: PubMed Central - PubMed

Affiliation: Service of Microbiology, Hospital Virgen de las Nieves, Granada, Spain.

Show MeSH
Related in: MedlinePlus