The binding of microorganisms to platelets is thought to be a major determinant of virulence in the pathogenesis of infective endocarditis. Previously, we demonstrated that a 23 kb chromosomal region is required for platelet binding by Streptococcus gordonii M99, a causative organism of infective endocarditis. The region contains a gene (gspB) encoding large cell wall anchoring protein and a 14 kb segment (the secY2/A2 locus) downstream of gspB. To assess the role of genes in the gspB-secY2/A2 locus, we have investigated the effects of a disruption of each gene on the surface expression of GspB in S. gordonii M99 and the platelet binding by the strain. Our results demonstrate that genes in the gspB-secY2/A2 locus can be categorized into four functional groups: (i) a gene encoding the platelet adhesin (gspB); (ii) genes involved in GspB export (secY2, secA2,asp1-5); (iii) genes required for GspB glycosylation (gtfA, gtfB); and (iv) genes that affect the glycosylation of GspB (gly, nss). As asp1-3, gtfA and gtfB are conserved in the homologous loci of several staphylococcal and streptococcal species, these genes may also have crucial roles in the expression and export of GspB homologues in the other Gram-positive bacteria.
(Research Team for Bacterial/Parasitic Diseases, TEL +81-29-838-7743)
Reference:
- Takamatsu et al. (2004) Mol. Microbiol. 52:189-203.
- Takamatsu et al. (2004) J. Bacteriol. 186:7100-7111.
- Takamatsu et al. (2005) J. Bacteriol. 187:3878-3883.
