Bacteria engage in social behavior by communicating through a variety of mechanisms. One method of communication is contact-dependent growth inhibition (CDI), a phenomenon in which one bacterium binds and delivers a toxin to a closely related target cell, using the proteins CdiB and CdiA. This toxin blocks cell growth unless the target cell contains an immunity protein, CdiI. The CDI pathway is the process by which toxins are delivered and activated, using distinct target-cell proteins such as outer membrane receptors and inner membrane transporters. The first chapter of this thesis focuses on the CDI system from Burkholderia pseudomallei 1026b. We identify three genes whose products appear to be necessary for growth inhibition, and describe a potential CDI pathway for this system. The second chapter discusses the mechanism by which Escherichia coli EC93 binds target cells. Mutations in BamA, the CdiAEC93 receptor, are described. These mutations confer resistance to CDI and block cell-cell binding. Both chapters demonstrate the variety and species specificity of CDI growth inhibition pathways
