Cell division is the ultimate process for the propagation of bacteria, and FtsZ is an essential protein used by nearly all bacteria for this function. Chlamydiae belong to a small group of bacteria that lack the universal cell division protein FtsZ but still divide by binary fission. Chlamydial MreB is a member of the shape-determining MreB/Mbl family of proteins responsible for rod shape morphology in Escherichia coli Chlamydia also encodes a homolog of RodZ, an MreB assembly cytoskeletal protein that links MreB to cell wall synthesis proteins. We hypothesized that MreB directs cell division in Chlamydia and that chlamydial MreB could replace FtsZ function for cell division in E. coli Overexpression of chlamydial mreB-rodZ in E. coli induced prominent morphological changes with production of large swollen or oval bacteria, eventually resulting in bacterial lysis. Low-level expression of chlamydial mreB-rodZ restored viability of a lethal ΔmreB mutation in E. coli, although the bacteria lost their typical rod shape and grew as rounded cells. When FtsZ activity was inhibited by overexpression of SulA in the ΔmreB mutant of E. coli complemented with chlamydial mreB-rodZ, spherical E. coli grew and divided. Localization studies using a fluorescent fusion chlamydial MreB protein indicated that chlamydial RodZ directs chlamydial MreB to the E. coli division septum. These results demonstrate that chlamydial MreB, in partnership with chlamydial RodZ, acts as a cell division protein. Our findings suggest that an mreB-rodZ-based mechanism allows Chlamydia to divide without the universal division protein FtsZ.IMPORTANCE The study of Chlamydia growth and cell division is complicated by its obligate intracellular nature and biphasic lifestyle. Chlamydia also lacks the universal division protein FtsZ. We employed the cell division system of Escherichia coli as a surrogate to identify chlamydial cell division proteins. We demonstrate that chlamydial MreB, together with chlamydial RodZ, forms a cell division and growth complex that can replace FtsZ activity and support cell division in E. coli Chlamydial RodZ plays a major role in directing chlamydial MreB localization to the cell division site. It is likely that the evolution of chlamydial MreB and RodZ to form a functional cell division complex allowed Chlamydia to dispense with its FtsZ-based cell division machinery during genome reduction. Thus, MreB-RodZ represents a possible mechanism for cell division in other bacteria lacking FtsZ.

中文翻译：

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在缺乏 FtsZ 活性的情况下，衣原体 MreB 可指导大肠杆菌中的细胞分裂和肽聚糖合成。


细胞分裂是细菌繁殖的最终过程，而 FtsZ 是几乎所有细菌用于实现此功能的必需蛋白质。衣原体属于一小类细菌，它们缺乏通用细胞分裂蛋白 FtsZ，但仍通过二元裂变进行分裂。衣原体 MreB 是形状决定蛋白 MreB/Mbl 家族的成员，负责大肠杆菌中的杆状形态。衣原体还编码 RodZ 的同源物，RodZ 是一种将 MreB 与细胞壁合成蛋白连接的 MreB 组装细胞骨架蛋白。我们假设 MreB 指导衣原体中的细胞分裂，并且衣原体 MreB 可以取代大肠杆菌中细胞分裂的 FtsZ 功能。大肠杆菌中衣原体 mreB-rodZ 的过度表达引起显着的形态变化，产生大的肿胀或椭圆形细菌，最终导致细菌裂解。衣原体 mreB-rodZ 的低水平表达恢复了大肠杆菌中致命的 ΔmreB 突变的活力，尽管细菌失去了其典型的杆状形状并生长为圆形细胞。当 FtsZ 活性被衣原体 mreB-rodZ 互补的大肠杆菌 ΔmreB 突变体中 SulA 的过表达抑制时，球形大肠杆菌生长并分裂。使用荧光融合衣原体 MreB 蛋白进行的定位研究表明，衣原体 RodZ 将衣原体 MreB 引导至大肠杆菌分裂隔膜。这些结果表明，衣原体 MreB 与衣原体 RodZ 一起发挥细胞分裂蛋白的作用。我们的研究结果表明，基于 mreB-rodZ 的机制允许衣原体在没有通用分裂蛋白 FtsZ 的情况下进行分裂。 重要性 衣原体生长和细胞分裂的研究因其专性细胞内性质和双相生活方式而变得复杂。 衣原体还缺乏通用分裂蛋白 FtsZ。我们利用大肠杆菌的细胞分裂系统作为替代来鉴定衣原体细胞分裂蛋白。我们证明，衣原体 MreB 与衣原体 RodZ 一起形成细胞分裂和生长复合物，可以取代 FtsZ 活性并支持大肠杆菌中的细胞分裂。衣原体 RodZ 在引导衣原体 MreB 定位到细胞分裂位点方面发挥着重要作用。衣原体 MreB 和 RodZ 的进化很可能形成功能性细胞分裂复合物，使得衣原体在基因组缩减过程中无需使用基于 FtsZ 的细胞分裂机制。因此，MreB-RodZ 代表了缺乏 FtsZ 的其他细菌的细胞分裂的可能机制。