BslA, a pXO1-encoded adhesin of Bacillus anthracis.
The Gram-positive pathogen Bacillus anthracis causes anthrax, a fulminant and lethal infection of mammals. Two large virulence plasmids, pXO1 and pXO2, harbour genes required for anthrax pathogenesis and encode secreted toxins or provide for the poly gamma-d-glutamic acid capsule. In addition to capsule, B. anthracis harbours additional cell wall envelope structures, including the surface layer (S-layer), which is composed of crystalline protein arrays. We sought to identify the B. anthracis envelope factor that mediates adherence of vegetative forms to human cells and isolated BslA (B. anthracisS-layer protein A). Its structural gene, bslA, is located on the pXO1 pathogenicity island (pXO1-90) and bslA expression is both necessary and sufficient for adherence of vegetative forms to host cells. BslA assembly into S-layers and surface exposure is presumably mediated by three N-terminal SLH domains. Twenty-three B. anthracis genes, whose products harbour similar SLH domains, may provide additional surface molecules that allow bacilli to engage cells or tissues of specific hosts during anthrax pathogenesis.
Kern
Justin W
JW
Department of Microbiology, University of Chicago, 920 East 58th Street, Chicago, IL, USA.
Schneewind
Olaf
O
D018829:Adhesins, Bacterial / Q000235:genetics* / Q000378:metabolism; D001408:Bacillus anthracis / Q000235:genetics / Q000502:physiology*; D002460:Cell Line; D004847:Epithelial Cells / Q000382:microbiology; D005347:Fibroblasts / Q000382:microbiology; D005816:Genetic Complementation Test; D044404:Genomic Islands; D006801:Humans; D008562:Membrane Glycoproteins / Q000235:genetics* / Q000378:metabolism; D008954:Models, Biological; D010957:Plasmids; D037521:Virulence Factors / Q000235:genetics* / Q000378:metabolism
D018829:Adhesins, Bacterial; D008562:Membrane Glycoproteins; C055764:S-layer proteins; D037521:Virulence Factors