Escherichia coli has the ability to resist severe acid stress, as that encountered during transit through the host stomach, and this is instrumental to host gut colonization. The glutamate-based acid resistance (AR) system plays a major role in the protection of the cell from the deleterious effects of a high-proton-concentration environment. Structural genes of this system are gadA, gadB and gadC, which encode two glutamate decarboxylase isoforms and a glutamate/γ-aminobutyrate (GABA) antiporter, respectively. Glutamate decarboxylation leads to both proton consumption and production of GABA, a neutral compound exported via the GadC antiporter. Even though the gadA and gadBC genes are 2,1 Mb apart, their transcription is under the control of the same regulators: GadE, GadX, GadW, H-NS and RpoS. These regulators also affect the expression of 12 genes located in the acid fitness island (AFI). We have identified the GadX (GadW) binding site, a 42 bp sequence, in the regulatory regions of gadA, gadBC, slp, hdeAB, gadE and gadY. All are AFI genes, but gadBC. In my talk I will show the most recent results from in vivo and in vitro analyses aimed at fully characterizing the GadX regulon. In addition I will show biochemical data on the decarboxylase’s intracellular activation/inactivation process and on additional effectors involved in GABA export.
Glutamate-based acid resistance in Escherichia coli: biochemical and regulatory aspects / DE BIASE, Daniela. - ELETTRONICO. - (2010), pp. 22-22. (Intervento presentato al convegno Society for general microbiology Autumn meeting 2010 tenutosi a University of Nottingham, Jubilee Campus nel 6-9 september 2010).