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衣原体组装病原体突触劫持宿主内质网。

Chlamydiae assemble a pathogen synapse to hijack the host endoplasmic reticulum.

机构信息

Institute of Structural and Molecular Biology, Birkbeck & University College London, Malet Street, London, WC1E 7HX, UK.

出版信息

Traffic. 2012 Dec;13(12):1612-27. doi: 10.1111/tra.12002. Epub 2012 Sep 11.

Abstract

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.

摘要

衣原体是专性细胞内细菌病原体,在称为“包涵体”的特殊膜结合隔室中复制。包涵体膜是一个关键的宿主-病原体界面,但它与细胞器官的相互作用程度及其起源仍未得到明确界定。在这里,我们表明宿主内质网(ER)被特异性招募到包涵体中,并且关键的粗糙内质网(rER)蛋白在包涵体上富集并易位到包涵体中。rER 招募是衣原体协调的过程,独立于宿主运输发生。产生感染性后代需要完整的 ER,因为在感染早期 ER 空泡化会阻止包涵体的发育,而在 rER 招募后破坏会使包涵体破裂。对感染衣原体的细胞进行电子断层扫描和免疫标记显示,在“病原体突触”处,有序排列的衣原体 III 型分泌复合物仅在 rER 接触部位与包涵体膜相连。我们的数据显示了一种参与病原体劫持关键宿主细胞器的超分子组装。

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