Previous Article | Next Article ![]()
Journal of Bacteriology, October 2003, p. 5925-5935, Vol. 185, No. 20
0021-9193/03/$08.00+0 DOI: 10.1128/JB.185.20.5925-5935.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.
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:
Copyright © 2009 by the American Society for Microbiology. For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»