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Journal of Bacteriology, May 2001, p. 2888-2896, Vol. 183, No. 9
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.9.2888-2896.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Bap, a Staphylococcus aureus Surface
Protein Involved in Biofilm Formation
Carme
Cucarella,1
Cristina
Solano,2
Jaione
Valle,2
Beatriz
Amorena,2
Íñigo
Lasa,2 and
José R.
Penadés1,*
Unit of Biochemistry, Department of Basic
Biomedical Sciences, Cardenal Herrera-CEU University, 46113 Moncada,
Valencia,1 and Instituto de
Agrobiotecnología y Recursos Naturales and Departamento de
Producción Agraria, Universidad Pública de Navarra-Consejo
Superior de Investigaciones Científicas, Campus de
Arrosadía, 31006 Pamplona,2 Spain
Received 20 October 2000/Accepted 7 February 2001
Identification of new genes involved in biofilm formation is needed
to understand the molecular basis of strain variation and the
pathogenic mechanisms implicated in chronic staphylococcal infections.
A biofilm-producing Staphylococcus aureus isolate was used
to generate biofilm-negative transposon (Tn917) insertion mutants. Two
mutants were found with a significant decrease in attachment to inert
surfaces (early adherence), intercellular adhesion, and biofilm
formation. The transposon was inserted at the same locus in both
mutants. This locus (bap [for biofilm associated protein]) encodes a novel cell wall associated protein of 2,276 amino
acids (Bap), which shows global organizational similarities to surface
proteins of gram-negative (Pseudomonas aeruginosa and Salmonella enterica serovar Typhi) and gram-positive
(Enteroccocus faecalis) microorganisms. Bap's core region
represents 52% of the protein and consists of 13 successive nearly
identical repeats, each containing 86 amino acids. bap was
present in a small fraction of bovine mastitis isolates (5% of the 350 S. aureus isolates tested), but it was absent from the 75 clinical human S. aureus isolates analyzed. All
staphylococcal isolates harboring bap were highly adherent
and strong biofilm producers. In a mouse infection model
bap was involved in pathogenesis, causing a persistent infection.
*
Corresponding author. Mailing address: Veterinary
School, Cardenal Herrera-CEU University, Edificio seminario, 46113 Moncada, Valencia, Spain. Phone: 34-96-1369000. Fax: 34-96-1395272. E-mail: jpenades{at}uch.ceu.es.
Journal of Bacteriology, May 2001, p. 2888-2896, Vol. 183, No. 9
0021-9193/01/$04.00+0 DOI: 10.1128/JB.183.9.2888-2896.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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