Fig. 7: fimH mutants display higher capacity to form biofilms and enhanced tolerance towards a lethal concentration of amikacin.

a, b Biofilm amounts (a) and colony forming units (b) of fimH mutants formed on silicone coupons for 24 h. c The survival rate of biofilm cells of fimH mutants on silicone coupons after the treatment with 80xMIC of AMK. It was calculated by using the formula 100x(CFU_AFTER/CFU_BEFORE), where CFU_BEFORE corresponds to CFU/coupon before treatment and CFU_AFTER to CFU/coupon after treatment. The data corresponded to n = 18 biological replicates for a, and n = 9 for b and c. Data are represented as the mean ± SD. Statistics correspond to unpaired two tailed t-test with Welch’s correction comparing each fimH mutant to its corresponding wt isogenic strain. *p < 0.05; **p < 0.01; ***p < 0.001, ****p < 0.0001. In c, statistics were performed on log-transformed % survival. fimH ∆29-40 in frame deletion is present in clone 239 that differs from the ancestral strain by this single mutation. We showed previously that the exact same fimH ∆29-40 deletion enhanced biofilm formation in E. coli K12⁵⁰ (see supplementary Data 4). The clone with the mutation fimH L79R was created after de-construction of the fusA G604V mutation from the clone 219 where we replaced the fusA G604V allele by a wt version of fusA (wtfusA-repair) (see Methods). This clone also codes for a synonymous mutation I255I in the gene LF82_RS22000.