SadB is a modulator of Pseudomonas aeruginosa PAO1 virulence

ABSTRACT: Pseudomonas aeruginosa sadB mutants exhibit a hyper-swarming but biofilm defective phenotype. To acquire insights into the contribution of sadB to virulence, we employed bioluminescence imaging and histopathology of mouse soft tissue infection. Compared with the parent PAO1 strain, the ΔsadB mutant was highly attenuated and rapidly cleared from the infection site whereas genetic complementation conferring constitutive expression of sadB resulted in a more invasive phenotype than the parent strain. Transcriptome analysis via RNA-seq of exponential and stationary phase planktonic cells revealed that SadB has a more global role than previously appreciated and acts as a pleiotropic regulator of diverse genes involved in biofilm development, quorum sensing (QS), secondary metabolite production, iron acquisition, virulence, protein secretion and anaerobiosis. In ΔsadB, we observed early induction of the rhl and pqs QS systems, increased production of siderophores and pyocyanin, changes in the expression of genes involved in c-diGMP signalling and a growth defect in under static but not shaking conditions. Since ΔsadB is a hyperswarmer and as swarming requires rhamnolipids, this suggested that deletion of sadB may impact on the timing and level of rhamnolipids produced. In ΔsadB, the rhlA and rhlB genes were induced in log rather than stationary phase resulting in overproduction of rhamnolipids likely as a consequence of the up-regulation of the rhl and pqs QS systems. Since rhamnolipids also contribute to biofilm maturation and dispersal and can act as anti-adhesives, we deleted the rhlA in ΔsadB and observed that biofilm formation was restored offering mechanistic insight into the biofilm defective phenotype of ΔsadB.

ORGANISM(S): Pseudomonas aeruginosa

PROVIDER: GSE302429 | GEO | 2026/03/09

REPOSITORIES: GEO