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Fig. 1 | BMC Microbiology

Fig. 1

From: The role of the two-component systems Cpx and Arc in protein alterations upon gentamicin treatment in Escherichia coli

Fig. 1

Organization and regulation of the Arc- and Cpx-TCS in E. coli. The Arc system is commonly induced under conditions provoking a reduced state of the quinone pool of the electron transport chain. The autophosphorylation of the SK ArcB is followed by a phosphoryl group transfer onto its cognate RR ArcA resulting in a specific response. The phosphorelay reaction for the phosphoryl group transfer from ArcB to ArcA is simplified for better understanding. The envelope stress sensing Cpx system is induced by e.g. misfolded proteins or nlpE overexpression, followed by autophosphorylation of CpxA, phosphotransfer onto its cognate RR CpxR and response of the cells. The Cpx system is inhibited by interaction of the periplasmic accessory protein CpxP with CpxA. As postulated by Kohanski et al. (2008) addition and uptake of aminoglycosides lead to mistranslation of proteins in the cytoplasm, and result in misfolded, periplasmic proteins activating the Cpx system [8]. According to this controversially discussed hypothesis, crosstalk between CpxA and ArcA takes place under this condition leading to cell death (red marked pathway). IM = inner membrane; OM = outer membrane

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