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Literature summary for 5.1.1.3 extracted from

  • Zhang, J.; Liu, J.; Ling, J.; Tong, Z.; Fu, Y.; Liang, M.
    Inactivation of glutamate racemase (MurI) eliminates virulence in Streptococcus mutans (2016), Microbiol. Res., 186-187, 1-8 .
    View publication on PubMed
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Application

Application Comment Organism
medicine MurI is a potentialtarget for controlling dental caries Streptococcus mutans serotype c

Cloned(Commentary)

Cloned (Comment) Organism
gene murI, quantitative real-time quantitative PCR expression analysis Streptococcus mutans serotype c

Protein Variants

Protein Variants Comment Organism
additional information inactivation of MurI eliminating the virulence in Streptococcus mutans. The length, width and height of strain FW1718 cells are increased by 1.7, 2.6, and 1.7fold, respectively. The murI mutant exhibits an enlarged cell size, longer cell chains, diminished cell-cell aggregation, and altered cell surface ultrastructure compared with the wild-type. Gene murI deficiency weakens acidogenicity, aciduricity, and biofilm formation ability of Streptococcus mutans. The deletion of murI reduces the expression of the acidogenesis-related gene ldh by 44fold. The expression levels of the gene coding for surface protein antigen P (spaP) and the acid-tolerance relatedgene (atpD) are downregulated by 99%. Expression of comE, comD, gtfB and gtfC genes, related to biofilm formation, are downregulated 8, 43, 85, and 298fold in the murI mutant compared with the wild-type, respectively Streptococcus mutans serotype c

Organism

Organism UniProt Comment Textmining
Streptococcus mutans serotype c Q8DSQ5
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Streptococcus mutans serotype c ATCC 700610 / UA159 Q8DSQ5
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Synonyms

Synonyms Comment Organism
MurI
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 Streptococcus mutans serotype c

General Information

General Information Comment Organism
malfunction inactivation of glutamate racemase eliminates the virulence in Streptococcus mutans, a stable mutant of Streptococcus mutans deficient in glutamate racemase, strain FW1718, is constructed to investigate the impact of murI inactivation on cariogenic virulence in wild-type strain UA159. The murI mutant exhibits an enlarged cell size, longer cell chains, diminished cell-cell aggregation, and altered cell surface ultrastructure compared with the wild-type. Gene murI deficiency weakens acidogenicity, aciduricity, and biofilm formation ability of Streptococcus mutans. The deletion of murI reduces the expression of the acidogenesis-related gene ldh by 44fold. The expression levels of the gene coding for surface protein antigen P (spaP) and the acid-tolerance related gene (atpD) are downregulated by 99%. Expression of comE, comD, gtfB and gtfC genes, related to biofilm formation, are downregulated 8, 43, 85, and 298fold in the murI mutant compared with the wild-type, respectively Streptococcus mutans serotype c
physiological function glutamate racemase (MurI) is an essential enzyme in peptidoglycan biosynthesis Streptococcus mutans serotype c