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. Author manuscript; available in PMC: 2016 Nov 20.
Published in final edited form as: J Mol Biol. 2015 Sep 24;427(23):3754–3765. doi: 10.1016/j.jmb.2015.09.010

Fig. 1. Contact-dependent growth inhibition (CDI).

Fig. 1

a) CDI+ bacteria carry cdiBAI gene clusters that encode CdiB-CdiA two-partner secretion proteins and CdiI immunity proteins. b) Model for the CdiB/CdiA complex. CdiB is represented by the crystal structure of B. pertussis FhaC (PDB: 3NJT), and CdiA is modeled as concatenated β-helices from E. coli Ag43 (PDB: 4KH3). c) CdiA binds to receptors on neighboring bacteria and delivers its C-terminal toxin domain (red star) into the target cell. If target cells lack immunity (left pathway), then their growth is inhibited. In contrast, CdiI neutralizes the toxin in isogenic CDI+ bacteria, preventing growth inhibition (right pathway).