A molecular understanding of bacterial disease is critical for the development of novel diagnostics and therapeutics, particularly given the increasing incidence of antibiotic resistance. Such studies also illuminate fundamental cellular mechanisms. The intracellular pathogen Chlamydia trachomatis replicates within a specialised compartment (inclusion), which is segregated from the endocytic pathway yet intercepts secretory traffic and engages organelles. The inclusion is extruded at the end of the replication cycle, but how this occurs remains unknown. Building on preliminary data, the project will investigate host and bacterial factors involved in chlamydial exit.
Hybiske K, Stephens RS (2007) Mechanisms of host cell exit by the intracellular bacterium Chlamydia. Proc Natl Acad Sci USA 104: 11430-
Taylor LD, Nelson DE, Dorward DW, Whitmire WM, Caldwell HD (2010) Biological characterization of Chlamydia trachomatis plasticity zone MACPF domain family protein CT153. Infect Immun 78:2691-
Law RH, Lukoyanova N, Voskoboinik I, Caradoc-Davies TT, Baran K, Dunstone MA, D'Angelo ME, Orlova EV, Coulibaly F, Verschoor S, Browne KA, Ciccone A, Kuiper MJ, Bird PI, Trapani JA, Saibil HR, Whisstock JC (2010) The structural basis for membrane binding and pore formation by lymphocyte perforin. Nature 468:447-
Nans A, Saibil HR, Hayward RD (2014) Pathogen-host reorganization during Chlamydia invasion revealed by cryo-electron tomography. Cell Microbiol 16:1457-