EC Number |
General Information |
Reference |
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1.14.13.149 | malfunction |
inhibition of quorum sensing by release of phenylacetic acid leads to attenuated virulence of the Burkholderia cenocepacia paaABCDE mutant. Burkholderia cenocepacia paaA and paaE mutants, in which the paaABCDE gene cluster is interrupted, are defective in PAA degradation and are attenuated for virulence in the nematode host model Caenorhabditis elegans. While the mutants of the PAA-CoA monooxygenase complex re attenuated for pathogenicity, mutants of the ring opening or beta-oxidation steps are not, possibly because some by-products are required for pathogenicity but not produced in DELTApaaABCDE. Phenotypes, overview |
-, 745801 |
1.14.13.149 | metabolism |
bifunctional PaaABCE acts as a phenylacetyl-CoA ring-1,2-epoxidase/ring-1,2-epoxyphenylacetyl-CoA deoxygenase |
-, 718163 |
1.14.13.149 | metabolism |
the enzyme complex is involved in the phenylacteic acid, PAA, degradation pathway, overview |
-, 745801 |
1.14.13.149 | physiological function |
loss of PaaABCDE decreases virulence. Deletion of either ligase PaaK or PaaABCDE leads to higher levels of released phenylacetic acid but no differences in levels of internal accumulation compared to the wild-type level. Removal of PaaABCDE in a LuxIR-like quorum sensing system CepR mutant does not impact its attenuated phenotype |
763958 |
1.14.13.149 | physiological function |
the phenylacetic acid degradation pathway of Burkholderia cenocepacia is active during cystic fibrosis-like conditions and is necessary for full pathogenicity of Burkholderia cenocepacia in nematode and rat infection models. Pathogenicity against Caenorhabditis elegans, increased with exogenous N-octanoyl-L-homoserine lactone |
-, 745801 |