Chlamydiae assemble a pathogen synapse to hijack the host endoplasmic reticulum.
Chlamydiae are obligate intracellular bacterial pathogens that replicate within a specialized membrane-bound compartment, termed an 'inclusion'. The inclusion membrane is a critical host-pathogen interface, yet the extent of its interaction with cellular organelles and the origin of this membrane remain poorly defined. Here we show that the host endoplasmic reticulum (ER) is specifically recruited to the inclusion, and that key rough ER (rER) proteins are enriched on and translocated into the inclusion. rER recruitment is a Chlamydia-orchestrated process that occurs independently of host trafficking. Generation of infectious progeny requires an intact ER, since ER vacuolation early during infection stalls inclusion development, whereas disruption post ER recruitment bursts the inclusion. Electron tomography and immunolabelling of Chlamydia-infected cells reveal 'pathogen synapses' at which ordered arrays of chlamydial type III secretion complexes connect to the inclusion membrane only at rER contact sites. Our data show a supramolecular assembly involved in pathogen hijack of a key host organelle.
Institute of Structural and Molecular Biology, Birkbeck & University College London, Malet Street, London, WC1E 7HX, UK.
Maud
M
Dumoux
Daniel K
DK
Clare
Helen R
HR
Saibil
Richard D
RD
Hayward
D001426:Bacterial Proteins / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D002692:Chlamydia trachomatis / Q000472:pathogenicity*; D004721:Endoplasmic Reticulum / Q000378:metabolism* / Q000382:microbiology; D006367:HeLa Cells; D054884:Host-Pathogen Interactions; D006801:Humans; D002479:Inclusion Bodies / Q000378:metabolism; D007425:Intracellular Membranes / Q000378:metabolism; D021381:Protein Transport; D022142:Secretory Vesicles / Q000378:metabolism; D014617:Vacuoles / Q000378:metabolism; D037521:Virulence Factors / Q000378:metabolism
D001426:Bacterial Proteins; D037521:Virulence Factors