A Chlamydia effector recruits CEP170 to reprogram host microtubule organization.
A Chlamydia effector recruits CEP170 to reprogram host microtubule organization.
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DOI：
10.1242/jcs.169318
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发表时间：
2015-09-15
影响因子：
4
通讯作者：
Hayward RD
中科院分区：
文献类型：
--
作者：
Dumoux M;Menny A;Delacour D;Hayward RD
专性细胞内细菌病原体沙眼衣原体（Chlamydia trachomatis）部署毒力效应子以破坏宿主细胞功能，从而使其能够在称为包涵体的专门的膜结合区室内复制。宿主细胞骨架的控制对于衣原体的摄取、包涵体的生物发生和细胞的退出是至关重要的。在这里，我们展示了衣原体效应如何重新安排微管（MT）网络启动组织的MT在夹杂物表面。我们确定了一个包含本地化的效应，足以干扰MT组装，我们命名为包含蛋白作用于MT（IPAM）。我们确定IPAM招募并刺激中心体蛋白170 kDa（CEP 170）劫持宿主细胞的MT组织功能。 我们表明，CEP170是必不可少的衣原体控制主机MT组件，并列入形态发生和细菌感染性。我们一起展示了病原体效应器如何重新编程宿主MT网络以支持其细胞内发育。沙眼衣原体是一种专性细胞内病原体。在这里，我们描述了衣原体毒力蛋白IPAM如何与宿主蛋白CEP170相互作用，以重编程宿主MT组织。
The obligate intracellular bacterial pathogen Chlamydia trachomatis deploys virulence effectors to subvert host cell functions enabling its replication within a specialized membrane-bound compartment termed an inclusion. The control of the host cytoskeleton is crucial for Chlamydia uptake, inclusion biogenesis and cell exit. Here, we demonstrate how a Chlamydia effector rearranges the microtubule (MT) network by initiating organization of the MTs at the inclusion surface. We identified an inclusion-localized effector that is sufficient to interfere with MT assembly, which we named inclusion protein acting on MTs (IPAM). We established that IPAM recruits and stimulates the centrosomal protein 170 kDa (CEP170) to hijack the MT organizing functions of the host cell. We show that CEP170 is essential for chlamydial control of host MT assembly, and is required for inclusion morphogenesis and bacterial infectivity. Together, we demonstrate how a pathogen effector reprograms the host MT network to support its intracellular development. Highlighted Article: Chlamydia trachomatis is an obligate intracellular pathogen. Here, we describe how the Chlamydia virulence protein IPAM interacts with the host protein CEP170 to reprogram host MT organization.