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The attenuated virulence of a B urkholderia cenocepacia paaABCDE mutant is due to inhibition of quorum sensing by release of phenylacetic acid
Author(s) -
Pribytkova Tanya,
Lightly Tasia Joy,
Kumar Brijesh,
Bernier Steve P.,
Sorensen John L.,
Surette Michael G.,
Cardona Silvia T.
Publication year - 2014
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.12771
Subject(s) - phenylacetic acid , quorum sensing , burkholderia cenocepacia , biology , microbiology and biotechnology , virulence , homoserine , mutant , biochemistry , gene
Summary 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.