Assembly and Development of the Pseudomonas aeruginosa Biofilm Matrix

By Luyan Z. Ma, M. Conover, Haiping Lu, M. Parsek, K. Bayles, D. Wozniak. PLoS Pathogens, 2009

673 citations recorded by the source corpus.

Virtually all cells living in multicellular structures such as tissues and organs are encased in an extracellular matrix. One of the most important features of a biofilm is the extracellular polymeric substance that functions as a matrix, holding bacterial cells together. Yet very little is known about how the matrix forms or how matrix components encase bacteria during biofilm development. Pseudomonas aeruginosa forms environmentally and clinically relevant biofilms and is a paradigm organism for the study of biofilms. The extracellular polymeric substance of P. aeruginosa biofilms is an ill-defined mix of polysaccharides, nucleic acids, and proteins. Here, we directly visualize the product of the polysaccharide synthesis locus (Psl exopolysaccharide) at different stages of biofilm development. During attachment, Psl is anchored on the cell surface in a helical pattern. This promotes cell–cell interactions and assembly of a matrix, which holds bacteria in the biofilm and on the surface. Chemical dissociation of Psl from the bacterial surface disrupted the Psl matrix as well as the biofilm structure. During biofilm maturation, Psl accumulates on the periphery of 3-D-structured microcolonies, resulting in a Psl matrix-free cavity in the microcolony center. At the dispersion stage, swimming cells appear in this matrix cavity. Dead cells and extracellular DNA (eDNA) are also concentrated in the Psl matrix-free area. Deletion of genes that control cell death and autolysis affects the formation of the matrix cavity and microcolony dispersion. These data provide a mechanism for how P. aeruginosa builds a matrix and subsequently a cavity to free a portion of cells for seeding dispersal. Direct visualization reveals that Psl is a key scaffolding matrix component and opens up avenues for therapeutics of biofilm-related complications.

Subfields: Genetics, Molecular Biology, Periodontics

View Paper: https://www.semanticscholar.org/paper/1ab02bb2b321af2110de298cd78779fb54182e08

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Citations in the corpus

Bacterial Extracellular Polysaccharides in Biofilm Formation and Function (2015, background): “PAO1 Δ psl mutants form thin, diffuse bio ﬁ lms lacking structure compared to the wild type PAO1, while the psl overexpressing strains form thicker bio ﬁ lms with signi ﬁ cantly more biomass and microcolony height (73).”
The biofilm matrix (2010, background): “During attachment, Psl is anchored to the cell surface in a helical pattern, possibly promoting cell–cell interaction”
Bacterial Biofilms: Development, Dispersal, and Therapeutic Strategies in the Dawn of the Postantibiotic Era (2013, background): “2005), thereby tailoring biofilm architecture to the specific environment (Sauer et al. 2004; Ma et al. 2009).”
Pseudomonas aeruginosa Lifestyle: A Paradigm for Adaptation, Survival, and Persistence (2017, background): “It is anchored around cells in a helical arrangement initiating biofilm formation by enhancing cell migration, cell-cell interaction and cell-surface adhesion whereas in mature biofilms it is located to the periphery of mushroom shaped macrocolonies (Ma et al., 2009; Zhao et al., 2013).”
Pseudomonas aeruginosa Biofilms (2020, background): “In a mature biofilm, Psl is located in peripheries of the mushroom-like structure where it helps maintain structural stability [22].”
Resistance of bacterial biofilms to disinfectants: a review (2011, background): “The formation and maintenance of mature biofilms are intimately linked to the production of an extracellular matrix (Branda et al. 2005; Ma et al. 2009).”
Biofilm Dispersal: Mechanisms, Clinical Implications, and Potential Therapeutic Uses (2010, background): “In P. aeruginosa, for example, strains that are deficient in the production of the Cid/Lrg toxin-antitoxin system produce biofilm colonies that do not undergo central hollowing (Webb et al., 2003; Ma et al., 2009).”
The role of bacterial biofilms in chronic infections (2013, background): “This suggests that dispersal, at least in vitro, is a controlled and not a stochastic event (59).”