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.
Chlamydiae assemble a pathogen synapse to hijack the host endoplasmic reticulum.
衣原体组装成病原体突触,劫持宿主内质网
阅读:11
作者:Dumoux Maud, Clare Daniel K, Saibil Helen R, Hayward Richard D
| 期刊: | Traffic | 影响因子: | 2.500 |
| 时间: | 2012 | 起止号: | 2012 Dec;13(12):1612-27 |
| doi: | 10.1111/tra.12002 | 研究方向: | 其它 |
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