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Journal of Bacteriology, September 2004, p. 5629-5639, Vol. 186, No. 17
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.17.5629-5639.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

The Enterococcus faecalis fsr Two-Component System Controls Biofilm Development through Production of Gelatinase

Lynn E. Hancock and Marta Perego*

Division of Cellular Biology, Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California

Received 2 April 2004/ Accepted 3 June 2004

Bacterial growth as a biofilm on solid surfaces is strongly associated with the development of human infections. Biofilms on native heart valves (infective endocarditis) is a life-threatening disease as a consequence of bacterial resistance to antimicrobials in such a state. Enterococci have emerged as a cause of endocarditis and nosocomial infections despite being normal commensals of the gastrointestinal and female genital tracts. We examined the role of two-component signal transduction systems in biofilm formation by the Enterococcus faecalis V583 clinical isolate and identified the fsr regulatory locus as the sole two-component system affecting this unique mode of bacterial growth. Insertion mutations in the fsr operon affected biofilm formation on two distinct abiotic surfaces. Inactivation of the fsr-controlled gene gelE encoding the zinc-metalloprotease gelatinase was found to prevent biofilm formation, suggesting that this enzyme may present a unique target for therapeutic intervention in enterococcal endocarditis.


* Corresponding author. Mailing address: Department of Molecular and Experimental Medicine, MEM-116, The Scripps Research Institute, 10550 North Torrey Pines Rd., La Jolla, CA 92037. Phone: (858) 784-7912. Fax: (858) 784-7966. E-mail: mperego{at}scripps.edu.


Journal of Bacteriology, September 2004, p. 5629-5639, Vol. 186, No. 17
0021-9193/04/$08.00+0     DOI: 10.1128/JB.186.17.5629-5639.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.




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