TABLE 2.
Summary of the role of LPS, EPS, motility, and RpoS in glass versus gallstone biofilms
| Mutant gene | Phenotype of gene mutant | Abilitya to form
biofilm on:
|
|
|---|---|---|---|
| Gallstone | Glass | ||
| phoP | Loss of PhoPQ two-component system | ++ | ++ |
| prgH | Loss of type III secretion apparatus | − | − |
| motA | Inability to rotate flagellum | + | − |
| fliA | Loss of flagellum | − | − |
| galE | Pleiotropic; EPS synthesis defect and loss of LPS O antigen | − | − |
| rfaD | Inability to add O antigen to LPS | + | − |
| bcs | Inability to synthesize cellulose EPS | + | − |
| wca | Inability to synthesize colanic acid EPS | + | + |
| rpoS | Loss of stationary-phase sigma factor | − | − |
a
Ability of strain to form a biofilm on gallstones as observed by SEM and on glass slides as observed by ruthenium red staining. ++, enhanced biofilm formation as compared to that by the wild type; −, severe defect in or complete loss of biofilm formation capability; +, normal wild-type biofilm formation.