Streptococcus gordonii's sequenced strain CH1 glucosyltransferase determines persistent but not initial colonization of teeth of rats.

Extracellular glucan synthesis from sucrose by Streptococcus gordonii, a major dental plaque biofilm bacterium, is assumed important for colonization of teeth; but this hypothesis is un-tested in vivo.To do so, we studied an isogenic glucosyltransferase (Gtf)-negative mutant (strain AMS12, gtfG(-)) of S. gordonii sequenced wild type (WT, strain Challis CH1, gtfG(+)), comparing their in vitro abilities to grow in the presence of glucose and sucrose and, in vivo, to colonize and persist on teeth and induce caries in rats. Weanling rats of two breeding colonies, TAN:SPFOM(OM)BR and TAN:SPFOM(OMASF)BR, eating high sucrose diet, were inoculated with either the WT (gtfG(+)), its isogenic gtfG(-) mutant, or reference strains of Streptococcus mutans. Control animals were not inoculated.In vitro, the gtfG(-) strain grew at least as rapidly in the presence of sucrose as its WT gtfG(+) progenitor, but formed soft colonies on sucrose agar, consistent with its lack of insoluble glucan synthesis. It also had a higher growth yield due apparently to its inability to channel carbon flow into extracellular glucan. In vivo, the gtfG(-) mutant initially colonized as did the WT but, unlike the WT, failed to persist on the teeth as shown over time. By comparison to three S. mutans strains, S. gordonii WT, despite its comparable ecological success on the teeth, was associated with only modest caries induction. Failure of the gtfG(-) mutant to persistently colonize was associated with slight diminution of caries scores by comparison with its gtfG(+) WT.Initial S. gordonii colonization does not depend on Gtf-G synthesis; rather, Gtf-G production determines S. gordonii's ability to persist on the teeth of sucrose-fed rats. S. gordonii appears weakly cariogenic by comparison with S. mutans reference strains.