Anticipating an alkaline stress through the Tor phosphorelay system in Escherichia coli.

The torCAD operon encoding the TMAO reductase respiratory system is induced in the presence of TMAO by the two-component regulatory system TorS/TorR. The TorS sensor detects TMAO and transphosphorylates the TorR response regulator via a four-step phosphorelay. Once phosphorylated, TorR activates expression of the torCAD structural operon. In order to identify new genes regulated by the Tor regulatory system, we performed a genome-wide transcriptional analysis by using the DNA array technology. We identified seven new transcriptional units whose expression is modulated by the TorS/TorR phosphorelay system. One unit, tnaLAB, is positively regulated whereas the other six, gadA, gadBC, hdeAB, hdeD, yhiE and yhiM, are negatively regulated by this system. Interestingly, the products of some of these units seem to play a role in the survival of E. coli in conditions of extreme pH. The TnaA tryptophanase has been proposed to counteract alkaline stress, whereas the GadA and GadB glutamate decarboxylases and the HdeA and HdeB proteins are involved in the defence against acid stress. Our hypothesis is that the TorS/TorR phosphorelay triggers alkaline-stress defence to limit alkalinization resulting from the reduction of TMAO in alkaline TMA by the Tor respiratory system. The fact that a DeltatnaLAB mutant showed a dramatic decrease in survival as a result of TMAO respiration is in agreement with such a model. As regulation of these genes by the TorS/TorR system does not depend on pH modification but rather on the presence of TMAO, we propose that E. coli anticipates alkalinization of the medium due to TMA production by base-resistance gene activation and acid-resistance gene repression.

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