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Abstract Biofilms are ubiquitous surface-associated bacterial communities embedded in an extracellular matrix. It is commonly assumed that biofilm cells are glued together by the matrix; however, how the specific biochemistry of matrix components affects the cell-matrix interactions and how these interactions vary during biofilm growth remain unclear. Here, we investigate cell-matrix interactions inVibrio cholerae, the causative agent of cholera. We combine genetics, microscopy, simulations, and biochemical analyses to show thatV. choleraecells are not attracted to the main matrix component (Vibriopolysaccharide, VPS), but can be attached to each other and to the VPS network through surface-associated VPS and crosslinks formed by the protein Bap1. Downregulation of VPS production and surface trimming by the polysaccharide lyase RbmB cause surface remodeling as biofilms age, shifting the nature of cell-matrix interactions from attractive to repulsive and facilitating cell dispersal as aggregated groups. Our results shed light on the dynamics of diverse cell-matrix interactions as drivers of biofilm development. 

The interaction between nanoparticles (NPs) and bacterial cell envelopes is crucial for designing effective antibacterial materials against multi-drug-resistant pathogens. However, the current understanding assumes a uniform bacterial cell wall. This study challenges that assumption by investigating how bacterial cell wall curvature impacts antibacterial NP action. Focusing on Janus NPs, which feature segregated hydrophobic and polycationic ligands and previously demonstrated high efficacy against diverse bacteria, we found that these NPs preferentially target and disrupt bacterial poles. Experimental and computational approaches reveal that curvature at E. coli poles induces conformational changes in lipopolysaccharide (LPS) polymers on the outer membrane, exposing underlying lipids for NP-mediated disruption. We establish that curvature-induced targeting by Janus NPs depends on the outer membrane composition and is most pronounced at physiologically relevant LPS densities. This work demonstrates that high-curvature regions of bacterial cell walls are “weak spots” for Janus NPs, thereby aiding the development of more effective targeted therapies. 

The anisotropic properties of Janus NPs are crucial for their ability to disrupt the negative-surface bacterial membrane modelviathe combination of hydrophobic and electrostatic interactions.