Deficiency of Glucan-binding Proteins Alters Gene Expression of Streptococcus mutans

Objective: Streptococcus mutans has been implicated as a major causative agent of dental caries in humans. Bacterial components associated with the adhesion phase of S. mutans include glucosyltransferases (GTFs; GTFB, GTFC, and GTFD), protein antigen c, and glucan binding proteins (Gbps; GbpA, GbpB, GbpC, and GbpD). Gbps have been shown to mediate the binding of glucans synthesized from sucrose by the action of GTFs, and several studies have found that the expression of genes including gtfs and gbps is regulated by quorum sensing genes. Recombinase A (RecA) was reported to be essential for recombination and repair of chromosomal DNA in Streptococcus pneumoniae and the recA gene, which encodes the RecA protein and is thought to be one of the quorum sensing genes of S. mutans. In the present study, we investigated whether Gbp deficiency has an effect on the interactions between Gbps and GTFs. Methods: GbpA-, GbpB-, and GbpC-deficient mutant strains (AD1, BD1, CD1, respectively) were constructed by insertional inactivation of corresponding genes of S. mutans MT8148 (serotype c). Next, the expression of GTF in Gbp isogenic mutants was determined using a reverse transcriptase polymerase chain reaction (RT-PCR) method, while protein expression profiles in Gbp-deficient mutant strains were investigated using two-dimensional gel electrophoresis (2-DE). Results: The RT-PCR assays showed that gtfB expression was elevated in AD1, while the expression of gtfD was decreased in CD1. In addition, expression of the recA gene was altered in the Gbp-deficient mutant strains, which was confirmed by the profiles of the expression proteins shown by 2-DE using those mutant strains. Conclusion: Our results suggest that Gbp deficiency has an effect on expression of the gtf gene, and indicate that stress response due to that deficiency influences recA gene expression and protein profiles in S. mutans.