Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, Connecticut, USA.
PLoS One. 2013;8(1):e54566. doi: 10.1371/journal.pone.0054566. Epub 2013 Jan 17.
The human pathogen Coxiella burnetii encodes a type IV secretion system called Dot/Icm that is essential for intracellular replication. The Dot/Icm system delivers bacterial effector proteins into the host cytosol during infection. The effector proteins delivered by C. burnetii are predicted to have important functions during infection, but when these proteins are needed during infection has not been clearly defined. Here, we use a reporter system consisting of fusion proteins that have a β-lactamase enzyme (BlaM) fused to C. burnetii effector proteins to study protein translocation by the Dot/Icm system. Translocation of BlaM fused to the effector proteins CBU0077, CBU1823 and CBU1524 was not detected until 8-hours after infection of HeLa cells, which are permissive for C. burnetii replication. Translocation of these effector fusion proteins by the Dot/Icm system required acidification of the Coxiella-containing vacuole. Silencing of the host genes encoding the membrane transport regulators Rab5 or Rab7 interfered with effector translocation, which indicates that effectors are not translocated until bacteria traffic to a late endocytic compartment in the host cell. Similar requirements for effector translocation were discerned in bone marrow macrophages derived from C57BL/6 mice, which are primary cells that restrict the intracellular replication of C. burnetii. In addition to requiring endocytic maturation of the vacuole for Dot/Icm-mediated translocation of effectors, bacterial transcription was required for this process. Thus, translocation of effector proteins by the C. burnetii Dot/Icm system occurs after acidification of the CCV and maturation of this specialized organelle to a late endocytic compartment. This indicates that creation of the specialized vacuole in which C. burnetii replicates represents a two-stage process mediated initially by host factors that regulate endocytic maturation and then by bacterial effectors delivered into host cells after bacteria establish residency in a lysosome-derived organelle.
人类病原体柯克斯体编码一种称为 Dot/Icm 的 IV 型分泌系统,该系统对于细胞内复制是必需的。Dot/Icm 系统在感染期间将细菌效应蛋白输送到宿主细胞质中。据预测,柯克斯体输送的效应蛋白在感染过程中具有重要功能,但这些蛋白在感染期间何时需要尚不清楚。在这里,我们使用一种由融合蛋白组成的报告系统来研究 Dot/Icm 系统的蛋白质转运,该融合蛋白将β-内酰胺酶(BlaM)与柯克斯体效应蛋白融合。直到 HeLa 细胞感染 8 小时后,才检测到 BlaM 融合到效应蛋白 CBU0077、CBU1823 和 CBU1524 上的转运,HeLa 细胞是柯克斯体复制的许可细胞。这些效应融合蛋白通过 Dot/Icm 系统的转运需要 Coxiella 包含的空泡酸化。宿主基因编码的膜转运调节剂 Rab5 或 Rab7 的沉默干扰了效应蛋白的转运,这表明效应蛋白只有在细菌运输到宿主细胞的晚期内体区室时才被转运。在源自 C57BL/6 小鼠的骨髓巨噬细胞中也发现了类似的效应蛋白转运要求,骨髓巨噬细胞是限制柯克斯体内在复制的原代细胞。除了需要空泡内体酸化来进行 Dot/Icm 介导的效应蛋白转运外,该过程还需要细菌转录。因此,柯克斯体 Dot/Icm 系统通过效应蛋白的转运需要 CCV 的酸化和这种特殊细胞器向晚期内体区室的成熟,这表明 Coxiella 复制所特有的空泡的创建代表了一个两阶段过程,最初由调节内体成熟的宿主因子介导,然后在细菌在溶酶体衍生的细胞器中定居后,由输送到宿主细胞的细菌效应蛋白介导。