| Autor: |
Pribytkova, Tanya, Lightly, Tasia Joy, Kumar, Brijesh, Bernier, Steve P., Sorensen, John L., Surette, Michael G., Cardona, Silvia T. |
| Předmět: |
|
| Zdroj: |
Molecular Microbiology; Nov2014, Vol. 94 Issue 3, p522-536, 15p, 2 Charts, 7 Graphs |
| Abstrakt: |
The phenylacetic acid degradation pathway of B urkholderia cenocepacia is active during cystic fibrosis-like conditions and is necessary for full pathogenicity of B . cenocepacia in nematode and rat infection models; however, the reasons for such requirements are unknown. Here, we show that the attenuated virulence of a phenylacetic acid catabolism mutant is due to quorum sensing inhibition. Unlike wild-type B . cenocepacia, a deletion mutant of the phenylacetyl- CoA monooxygenase complex (Δ paaABCDE) released phenylacetic acid in the medium that favours infection in C aenorhabditis elegans. Addition of phenylacetic acid further decreased the pathogenicity of the Δ paaABCDE, which cannot metabolize phenylacetic acid, but did not affect the wild-type, due to phenylacetic acid consumption. In line with reduced detection of acyl-homoserine lactones in spent medium, the Δ paaABCDE exhibited transcriptional inhibition of the quorum sensing system cepIR. Phenotypes repressed in Δ paaABCDE, protease activity and pathogenicity against C . elegans, increased with exogenous N-octanoyl-L-homoserine lactone. Thus, we demonstrate that the attenuated phenotype of B . cenocepacia Δ paaABCDE is due to quorum sensing inhibition by release of phenylacetic acid, affecting N-octanoyl-L-homoserine lactone signalling. Further, we propose that active degradation of phenylacetic acid by B . cenocepacia during growth in cystic fibrosis-like conditions prevents accumulation of a quorum sensing inhibiting compound. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
|
Plný text