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PMID:8359902
| Citation |
Yamashita, Y, Bowen, WH, Burne, RA and Kuramitsu, HK (1993) Role of the Streptococcus mutans gtf genes in caries induction in the specific-pathogen-free rat model. Infect. Immun. 61:3811-7 |
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| Abstract |
The role of each of the Streptococcus mutans gtf genes coding for glucan synthesis in cariogenesis was evaluated by using strain UA130 in the specific-pathogen-free (SPF) rat model system. Mutants defective in either or both of the genes required for insoluble glucan synthesis, the gtfB and gtfC genes, exhibited markedly reduced levels of smooth-surface carious lesions relative to that of the parental organism. Likewise, the mutant defective in the gtfD gene coding for the glucosyltransferase-S enzyme synthesizing water-soluble glucans also produced significantly fewer smooth-surface lesions than strain UA130. None of these mutations markedly altered the rate of sulcal caries induction relative to that of the parental organism. In addition, a mutant of strain UA130 defective in the gtfA gene was reexamined in the SPF rat model. In contrast to previous results from a gnotobiotic rat system, these mutants also induced significantly fewer smooth-surface carious lesions compared with that by strain UA130. These results suggest that all four genes are important for smooth-surface caries formation. Furthermore, these results are discussed relative to the differences in the diets utilized in the SPF and gnotobiotic rat model systems for assessing the virulence factors of S. mutans. |
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| Keywords |
Animals; Dental Caries/microbiology; Genes, Bacterial; Glucosyltransferases/genetics; Mutation; Polysaccharides/biosynthesis; Rats; Rats, Sprague-Dawley; Specific Pathogen-Free Organisms; Streptococcus mutans/genetics; Streptococcus mutans/pathogenicity |
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Significance
Annotations
| Gene product | Qualifier | GO Term | Evidence Code | with/from | Aspect | Extension | Notes | Status |
|---|---|---|---|---|---|---|---|---|
| GO:0009250: glucan biosynthetic process |
ECO:0000314: |
P |
GtfB gene mutants made by insertion and deletion into plasmid. GtfB mutants exhibited only 69% of wild-type capacity for insoluble glucan formation. Inferred from Western blot. |
complete | ||||
See also
References
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