Inactivation of glutamate racemase (MurI) eliminates virulence in Streptococcus mutans.

摘要: Inhibition of enzymes required for bacterial cell wall synthesis is often lethal or leads to virulence defects. Glutamate racemase (MurI), an essential enzyme in peptidoglycan biosynthesis, has been attractive target therapeutic interventions. Streptococcus mutans, one the many etiological factors dental caries, possesses a series associated with cariogenicity. However, little known regarding mechanism by which MurI influences pathogenesis S. mutans. In this work, stable mutant mutans deficient glutamate (S. FW1718) was constructed investigate impact murI inactivation on cariogenic UA159. Microscopy revealed that exhibited enlarged size, longer chains, diminished cell⬜cell aggregation, and altered surface ultrastructure compared wild-type. Characterization deficiency weakened acidogenicity, aciduricity, biofilm formation ability (P<0.05). Real-time quantitative polymerase chain reaction (qRT-PCR) analysis demonstrated deletion reduced expression acidogenesis-related gene ldh 44-fold (P<0.0001). The levels coding protein antigen P (spaP) acid-tolerance related (atpD) were down-regulated 99% Expression comE, comD, gtfB gtfC, genes formation, 8-, 43-, 85- 298-fold wild-type (P<0.0001), respectively. Taken together, current study provides first evidence adversely affects properties, making potential controlling caries.