Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, USA.
Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts, USA
J Bacteriol. 2018 Aug 24;200(18). doi: 10.1128/JB.00230-18. Print 2018 Sep 15.
Individual cells of the bacterium can elongate up to 40-fold on surfaces before engaging in a cooperative surface-based motility termed swarming. How cells regulate this dramatic morphological remodeling remains an open question. In this paper, we move forward the understanding of this regulation by demonstrating that requires the gene for swarmer cell elongation and subsequent swarm motility. The gene encodes a protein homologous to the dTDP-glucose 4,6-dehydratase protein of , which contributes to enterobacterial common antigen biosynthesis. Here, we characterize the gene in , demonstrating that it is required for the production of large lipopolysaccharide-linked moieties necessary for wild-type cell envelope integrity. We show that the absence of the gene induces several stress response pathways, including those controlled by the transcriptional regulators RpoS, CaiF, and RcsB. We further show that in -deficient cells, the suppression of the Rcs phosphorelay, via loss of RcsB, is sufficient to induce cell elongation and swarm motility. However, the loss of RcsB does not rescue cell envelope integrity defects and instead results in abnormally shaped cells, including cells producing more than two poles. We conclude that an RcsB-mediated response acts to suppress the emergence of shape defects in cell envelope-compromised cells, suggesting an additional role for RcsB in maintaining cell morphology under stress conditions. We further propose that the composition of the cell envelope acts as a checkpoint before cells initiate swarmer cell elongation and motility. swarm motility has been implicated in pathogenesis. We have found that cells deploy multiple uncharacterized strategies to handle cell envelope stress beyond the Rcs phosphorelay when attempting to engage in swarm motility. While RcsB is known to directly inhibit the master transcriptional regulator for swarming, we have shown an additional role for RcsB in protecting cell morphology. These data support a growing appreciation that the Rcs phosphorelay is a multifunctional regulator of cell morphology in addition to its role in microbial stress responses. These data also strengthen the paradigm that outer membrane composition is a crucial checkpoint for modulating entry into swarm motility. Furthermore, the -dependent moieties provide a novel attractive target for potential antimicrobials.
单个细菌细胞可以在表面上伸长至 40 倍，然后进行称为群集运动的合作表面运动。细胞如何调节这种剧烈的形态重塑仍然是一个悬而未决的问题。在本文中，我们通过证明需要基因来进行 swarmer 细胞伸长和随后的群集运动，从而推进了对这种调节的理解。该基因编码一种与 的 dTDP-葡萄糖 4,6-脱水酶蛋白同源的蛋白质，该蛋白有助于肠杆菌共同抗原的生物合成。在这里，我们对进行了表征，证明它是产生大的脂多糖连接部分所必需的，这些部分对于野生型细胞包膜完整性是必需的。我们表明，基因的缺失会诱导几种应激反应途径，包括受转录调节剂 RpoS、CaiF 和 RcsB 控制的途径。我们进一步表明，在缺陷细胞中，通过丧失 RcsB 抑制 Rcs 磷酸传递，足以诱导细胞伸长和群集运动。然而，RcsB 的缺失不能挽救细胞包膜完整性缺陷，反而导致异常形状的细胞，包括产生超过两个极的细胞。我们得出的结论是，RcsB 介导的反应作用是抑制细胞包膜受损细胞中形态缺陷的出现，这表明 RcsB 在应激条件下维持细胞形态方面具有额外的作用。我们进一步提出，细胞 envelope 的组成在细胞开始 swarmer 细胞伸长和运动之前充当检查点。 swarm motility 已被牵连到发病机制中。我们发现，当试图进行 swarm motility 时，细胞会采用多种未被表征的策略来处理细胞 envelope 应激，而不仅仅是 Rcs 磷酸传递。虽然 RcsB 已知可直接抑制 swarm 的主转录调节剂，但我们已经显示出 RcsB 在保护细胞形态方面的额外作用。这些数据支持这样一种观点，即 Rcs 磷酸传递除了在微生物应激反应中的作用外，还是细胞形态的多功能调节剂。这些数据还加强了这样一种观点，即外膜组成是调节进入群集运动的关键检查点。此外，基因依赖性部分为潜在的抗菌药物提供了一个新的有吸引力的目标。
