Films of Bacteria at Interfaces (FBI): Remodeling of Fluid Interfaces by Pseudomonas aeruginosa

TL;DR

This study compares the behaviors of two Pseudomonas aeruginosa strains at oil-water interfaces, revealing genetic and metabolic factors involved in elastic film formation and bacterial adaptation to interface stresses.

Contribution

It uncovers the genetic and metabolic mechanisms, especially alkB2's role, underlying elastic film formation by Pseudomonas aeruginosa at fluid interfaces, differing from traditional biofilms.

Findings

PAO1 forms elastic bacterial films at interfaces.

PA14 moves actively without forming elastic films.

alkB2 gene is crucial for elastic film formation.

Abstract

Bacteria at fluid interfaces endure physical and chemical stresses unique to these highly asymmetric environments. The responses of Pseudomonas aeruginosa PAO1 and PA14 to a hexadecane-water interface are compared. PAO1 cells form elastic films of bacteria, excreted polysaccharides and proteins, whereas PA14 cells move actively without forming an elastic film. Studies of PAO1 mutants show that, unlike solid-supported biofilms, elastic interfacial film formation occurs in the absence of flagella, pili, or certain polysaccharides. Highly induced genes identified in transcriptional profiling include those for putative enzymes and a carbohydrate metabolism enzyme, alkB2; this latter gene is not upregulated in PA14 cells. Notably, PAO1 mutants lacking the alkB2 gene fail to form an elastic layer. Rather, they form an active film like that formed by PA14. These findings demonstrate that genetic expression is altered by interfacial confinement, and suggest that the ability to metabolize alkanes may play a role in elastic film formation at oil-water interfaces.