Stress response to aromatic compounds in Acinetobacter radioresistens S13

Acinetobacter radioresistens S13 is a strain selected for its ability in phenol degradation. It is also able to degrade other aromatic compounds (i.e., Benzoate) through the b-ketoadipate pathway(1). Comparative proteomics alkaline studies on bacterium grown either on phenol or benzoate as sole carbon source reveal a different response to stress induced by these two aromatic compounds. Phenol is a solvent able to solubilize outer membrane lipoproteins, lipooligosaccharides (LOS) and phosphatidylethanolamine, damaging cell wall (2). This compound induces an overexpression of two proteases (ClpX and Serine protease) and of two RNA polymerase modulator factors (NusA and Rho)suggesting a gene modulation based on rE regulation. Instead benzoate induces an alternative phosphorylation-dependent stress-sensing response, maintained by a two-component regulatory system, which consist of a membrane-embedded sensory kinase and a response regulator (3). The kinase auto-phosphorylates a conserved histidine on the receipt of a stress-signal before transferring the phosphoryl group to an invariant aspartate in its cognate response regulator and in doing so activates its latent biological function (4).