Identify the cause of impaired surface attachment when earlier stages are disrupted

Ascertain whether the impaired surface attachment observed in Escherichia coli mutants that disrupt rosette formation or multicellular extension results from the necessity of sequential stage-specific gene regulation or from a requirement that type-1 fimbriae, curli, and Antigen 43 function in concert with poly-β-1,6-N-acetyl-D-glucosamine during attachment.

Background

E. coli self-organization culminates in surface attachment and cessation of growth, mediated by production of the extracellular polysaccharide PGA. Mutations affecting earlier stages (Ag43- or flagella-dependent rosette formation; fimbriae- or curli-dependent extension) also reduce attachment in communities formed by aggregation, leaving unclear whether attachment failure reflects disrupted stage-specific regulation or a structural requirement for multiple adhesins to act together with PGA.