Effect of disruption of a gene encoding an autolysin of Enterococcus faecalis OG1RF.

TitleEffect of disruption of a gene encoding an autolysin of Enterococcus faecalis OG1RF.
Publication TypeJournal Article
Year of Publication1998
AuthorsQin, X, Singh, KV, Xu, Y, Weinstock, GM, Murray, BE
JournalAntimicrob Agents Chemother
Date Published1998 Nov
KeywordsAnimals, Enterococcus faecalis, Female, Mice, Mice, Inbred ICR, Mutation, N-Acetylmuramoyl-L-alanine Amidase, Penicillins, Peritonitis, Virulence

A mutant (TX5127) of Enterococcus faecalis OG1RF was generated by disruption mutagenesis of a previously described autolysin gene. TX5127 formed longer chains (2 to 10 cells per chain) than wild-type OG1RF (mainly single cells) during growth in broth even though it had a growth rate similar to that of the parental strain as measured by turbidity and cell count. Autolysin activity, as defined by the ability to lyse heat-killed Micrococcus lysodeikticus cells, was absent in TX5127, while this activity was easily detectable in OG1RF. However, disruption of this autolysin gene did not block the ability of TX5127 to hydrolyze E. faecalis cell walls compared to that of OG1RF. The autolysis rate of cells of TX5127 in 10 mM sodium phosphate buffer (pH 6.8) was slower than that of wild-type OG1RF. TX5127 also showed a decreased rate of lysis in the presence of penicillin, as measured by changes in the turbidity of the culture during 24 h of incubation at 37 degrees C and a slightly decreased effect of penicillin as measured by time-kill curves. The virulence of TX5127 was similar to that of OG1RF in the mouse peritonitis model, indicating that the autolysin of E. faecalis is not important for infection in this model.

Alternate JournalAntimicrob. Agents Chemother.
PubMed ID9797220
PubMed Central IDPMC105960
Grant ListAI33516 / AI / NIAID NIH HHS / United States