Figure 2.
Two signaling pathways for extracytoplasmic stress responses in E. coli. Components of these pathways reside on each side of the cytoplasmic membrane (periplasm and cytoplasm). In the presence of misfolded periplasmic proteins, an unknown mechanism triggers a conformational change of the CpxA that leads to an activation of its kinase activity and promote an increase in CpxR phosphorylation. Under normal physiological conditions, σE is sequestred by RseA and DegS is inactive, with its PDZ domain inhibiting the protease activity. Recognition by the PDZ domain of misfolded periplasmic proteins relieves inhibition of the DegS protease. Activated DegS cleaves RseA, which releases σE. For both signal transduction systems, a partial list of the downstream targets is indicated.