Project name: Streptococcus pneumoniae

Description: Despite vaccines, S. pneumoniae kills more than a million people yearly. Thus, understanding how pneumococci transition from commensal to pathogen is particularly relevant. Quorum-sensing regulates collective behaviors, and as such represent potential drivers of commensal-to-pathogen transitions. In streptococci, Rgg/SHP quorum-sensing systems are widespread; yet, they remain largely uncharacterized in S. pneumoniae. Using directional RNA-seq, we show that the S. pneumoniae D39 Rgg0939/SHP system induces transcription of a single gene cluster, including shp, and capsule gene homologs. Capsule size measurements determined by FITC-dextran exclusion allowed the assignment of the system to regulation of surface polysaccharide expression. We found that the SHP pheromone induced exopolysaccharide expression in R36A, an unencapsulated derivative of D39. In the encapsulated parent strain, overexpression of the Rgg system resulted in a mutant with increased capsule size, whereas deletion of the system had no significant effect. In line with previous findings that capsule expression is inversely associated with biofilm formation, we found that biofilm formed on lung epithelial cells was increased in the rgg deletion mutant, and decreased in the overexpression strain. Surprisingly, no significant differences were observed between D39 and the rgg deletion mutant in a mouse model of lung infection, which may indicate redundancy of the system. This is the first study to reveal a quorum-sensing system in streptococci that regulates exopolysaccharide synthesis from a site distinct from the original capsule locus.

Data type: raw sequence reads

Sample scope: Monoisolate

Relevance: Medical

Last updated: 2017-03-02