This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sapunaric, F. Articles by Coyette, J. Search for Related Content PubMed PubMed Citation Articles by Sapunaric, F. Articles by Coyette, J.

Redefining the Role of psr in ß-Lactam Resistance and Cell Autolysis of Enterococcus hirae

Department of Molecular Biology and Microbiology, School of Medicine, Tufts University, Boston, Massachusetts 02111,¹ Centre d'Ingénierie des Protéines, Université de Liège, Institut de Chimie, B-4000 Liège, Belgium,² Laboratorio de Resistencia Bacteriana, Cátedra de Microbiologia, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires, Junin 956, 1113 Buenos Aires, Argentina,³ Genetics Unit, Shriners Hospital for Children, Montréal, Québec, Canada H3G 1A6⁴

Received 3 March 2003/ Accepted 28 July 2003

The contribution of penicillin-binding protein 5 (PBP5) and the PBP5 synthesis repressor (Psr) to the ß-lactam resistance, growth, and cell autolysis of wild-type strain ATCC 9790 and resistant strain R40 of Enterococcus hirae was investigated by disruption or substitution of the corresponding pbp5 and psr genes by Campbell-type recombination. The resulting modifications were confirmed by hybridization and PCR. The low susceptibility of E. hirae to ß-lactams was confirmed to be largely dependent on the presence of PBP5. However, against all expectations, inactivation of psr in ATCC 9790 or complementation of R40 cells with psr did not modify the susceptibility to benzylpenicillin or the growth and cell autolysis rates. These results indicated that the psr gene does not seem to be involved in the regulation of PBP5 synthesis and consequently in ß-lactam resistance or in the regulation of cell autolysis in E. hirae.

This article has been cited by other articles:

• Leimanis, S., Hoyez, N., Hubert, S., Laschet, M., Sauvage, E., Brasseur, R., Coyette, J. (2006). PBP5 Complementation of a PBP3 Deficiency in Enterococcus hirae.. J. Bacteriol. 188: 6298-6307 [Abstract] [Full Text]  
• Chatfield, C. H., Koo, H., Quivey,, R. G. Jr (2005). The putative autolysin regulator LytR in Streptococcus mutans plays a role in cell division and is growth-phase regulated. Microbiology 151: 625-631 [Abstract] [Full Text]