Institute of Biology, Humboldt-Universität zu Berlin, Philippstr. 13, 10115, Berlin, Germany.
Department of Microbiology, The Ohio State University, Columbus, OH, 43210, USA.
Nat Commun. 2024 Jul 14;15(1):5921. doi: 10.1038/s41467-024-50278-0.
The bacterial flagellum, which facilitates motility, is composed of ~20 structural proteins organized into a long extracellular filament connected to a cytoplasmic rotor-stator complex via a periplasmic rod. Flagellum assembly is regulated by multiple checkpoints that ensure an ordered gene expression pattern coupled to the assembly of the various building blocks. Here, we use epifluorescence, super-resolution, and transmission electron microscopy to show that the absence of a periplasmic protein (FlhE) prevents proper flagellar morphogenesis and results in the formation of periplasmic flagella in Salmonella enterica. The periplasmic flagella disrupt cell wall synthesis, leading to a loss of normal cell morphology resulting in cell lysis. We propose that FlhE functions as a periplasmic chaperone to control assembly of the periplasmic rod, thus preventing formation of periplasmic flagella.
细菌鞭毛可促进运动,由约 20 种结构蛋白组成,这些蛋白组装成一个长的细胞外丝状体,通过周质杆连接到细胞质转子-定子复合物上。鞭毛组装受到多个检查点的调节,这些检查点确保了有序的基因表达模式与各种构建块的组装相耦合。在这里,我们使用荧光显微镜、超分辨率显微镜和透射电子显微镜来表明周质蛋白(FlhE)的缺失会阻止鞭毛的正常形态发生,并导致沙门氏菌中周质鞭毛的形成。周质鞭毛会破坏细胞壁的合成,导致正常细胞形态的丧失,从而导致细胞裂解。我们提出 FlhE 作为周质分子伴侣发挥作用,以控制周质杆的组装,从而防止周质鞭毛的形成。