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. 2020 Oct 7;9:e56533. doi: 10.7554/eLife.56533

Figure 4. EPS composition drives biofilm and substrate deformations.

(A) Deformations of hydrogel substrates by V. cholerae Rg, rbma- and bap1- biofilms. Biofilms formed by rbma- and bap1- fail to deform the substrate. bap1- biofilms delaminate from the hydrogel surface. (B) Comparison of hydrogel deformations by P. aeruginosa Rg and cdrA- biofilms. (C) Dependence of maximum deformations on P. aeruginosa Rg, cdrA-, pel- and psl- biofilm diameter. All matrix mutants tend to generate weaker deformations compared to Rg. Data points correspond to different biofilms grown in two microfluidic chambers. (D) A model for the mechanism of biofilm deformation of soft substrates. Buildup of mechanical stress in the biofilm induces buckling. Adhesion between the biofilm and the surface transmits buckling-generated stress to the hydrogel, inducing deformations. E = 38 kPa. Scale bars: 20 µm.

Figure 4—source data 1. Deformation amplitude for PAO1 matrix mutants.

Figure 4.

Figure 4—figure supplement 1. Deformation behaviour for vpsL deletion mutant and complementation strains.

Figure 4—figure supplement 1.

(A) VpsL deletion mutant can not form biofilms. Complementation of (B) V. cholerae rbmA and (C) bap1 deletion mutants (brightfield, top) restore the ability of the biofilm to deform the hydrogel (reslice, bottom). E = 38 kPa. Scale bars: 20 µm.
Figure 4—figure supplement 2. P. aeruginosa biofilms on substrates with different stiffness.

Figure 4—figure supplement 2.

Increasing hydrogel stiffness to 200 kPa induces delamination of biofilms, as observed on glass. Scale bars: 20 µm.