The <i>Pseudomonas aeruginosa</i> Flagellar Cap Protein, FliD, Is Responsible for Mucin Adhesion

<jats:title>ABSTRACT</jats:title> <jats:p> Mucin-specific adhesion of <jats:italic>Pseudomonas aeruginosa</jats:italic> plays an important role in the initial colonization of this organism in the airways of cystic fibrosis patients. We report here that the flagellar cap protein, FliD, participates in this adhesion process. A polar chromosomal insertional mutation in the <jats:italic>P. aeruginosa fliD</jats:italic> gene made this organism nonadhesive to mucin in an in vitro mucin adhesion assay. The adhesive phenotype was restored by providing the <jats:italic>fliD</jats:italic> gene alone on a multicopy plasmid, suggesting involvement of this gene in mucin adhesion of <jats:italic>P. aeruginosa</jats:italic> . Further supporting this observation, the in vitro competition experiments demonstrated that purified FliD protein inhibited the mucin adhesion of nonpiliated <jats:italic>P. aeruginosa</jats:italic> PAK-NP, while the same concentrations of PilA and FlaG proteins of <jats:italic>P. aeruginosa</jats:italic> were ineffective in this function. The regulation of the <jats:italic>fliD</jats:italic> gene was studied and was found to be unique in that the transcription of the <jats:italic>fliD</jats:italic> gene was independent of the flagellar sigma factor ς <jats:sup>28</jats:sup> . Consistent with this finding, no ς <jats:sup>28</jats:sup> binding sequence could be identified in the <jats:italic>fliD</jats:italic> promoter region. The results of the β-galactosidase assays suggest that the <jats:italic>fliD</jats:italic> gene in <jats:italic>P. aeruginosa</jats:italic> is regulated by the newly described transcriptional regulator FleQ and the alternate sigma factor ς <jats:sup>54</jats:sup> (RpoN). </jats:p>