Hydrophobic surface exposure-mediated CIRCE repression by the Ca2+-sensor, HrcA, in Streptococcus pneumoniae

Heat shock-induced expression of the CIRCE (controlling inverted repeat of chaperone expression) regulon in Streptococcus pneumoniae was examined in the presence of Ca2+. In the presence of the Ca2+, thermo-resistance and expression of the CIRCE regulon of S. pneumoniae were significantly repressed. In addition, hydrophobicity of the HrcA was increased in the presence of the metal ion suggesting that Ca2+ induces conformational changes such as exposure of the hydrophobic surfaces of HrcA, which facilitate binding to GroEL. This in turn enhances access to CIRCE and leads to repression of the dnaK and groE operons.