Selection for nonspecific adhesion is a driver of FimH evolution increasing biofilm capacity.

Bacterial interactions with surfaces rely on the coordinated expression of a vast repertoire of surface-exposed adhesins. However, how bacteria dynamically modulate their adhesion potential to achieve successful surface colonization is not yet well understood. Here, we investigated changes in adhesion capacity of an initially poorly adherent strain using experimental evolution and positive selection for mutations improving adhesion and biofilm formation on abiotic surfaces. We showed that all identified evolved populations and clones acquired mutations located almost exclusively in the lectin domain of , the gene coding for the α-d-mannose-specific tip adhesin of type 1 fimbriae, a key virulence factor. While most of these mutants showed reduced mannose-binding ability, they all displayed enhanced binding to abiotic surfaces, indicating a trade-off between FimH-mediated specific and nonspecific adhesion properties. Several of the identified mutations were already reported in the FimH lectin domain of pathogenic and environmental , suggesting that, beyond pathoadaptation, FimH microevolution favoring nonspecific surface adhesion could constitute a selective advantage for natural isolates. Consistently, although deleted for the operon still evolves an increased adhesion capacity, mutants selected in the ∆ background are outcompeted by mutants revealing clonal interference for adhesion. Our study therefore provides insights into the plasticity of adhesion potential and shows that evolution of type 1 fimbriae is a major driver of the adaptation of natural to colonization.