The phenylacetic acid degradation pathway of Burkholderia cenocepacia is necessary for full pathogenicity of B. cenocepacia in nematode; however, the reasons of such requirements are unknown. Unlike wild type B. cenocepacia, a deletion mutant of the phenylacetyl-CoA monooxygenase complex (ΔpaaABCDE) released phenylacetic acid extracellularly in conditions that allow infection in Caenorhabditis elegans. Addition of phenylacetic acid further decreased the pathogenicity of the ΔpaaABCDE, which cannot metabolize phenylacetic acid, but did not affect the wild type, due to phenylacetic acid consumption. Detection of acyl-homoserine lactones was reduced in spent medium from ΔpaaABCDE compared to that of the wild type strain. Phenotypes repressed in ΔpaaABCDE, protease activity and pathogenicity against C. elegans, increased with the addition of exogenous N-octanoyl-L-homoserine lactone. Thus, it was demonstrated that the attenuated phenotype of B. cenocepacia ΔpaaABCDE is due to quorum sensing inhibition by release of phenylacetic acid, affecting N-octanoyl-L-homoserine lactone signaling. / October 2014
| Identifer | oai:union.ndltd.org:MANITOBA/oai:mspace.lib.umanitoba.ca:1993/23961 |
| Date | 03 September 2014 |
| Creators | Pribytkova, Tatiana |
| Contributors | Cardona, Silvia T.(Microbiology), Brassinga, Ann Karen (Microbiology) Sorensen, John L. (Chemistry) |
| Source Sets | University of Manitoba Canada |
| Detected Language | English |
Page generated in 0.0011 seconds