Mutations in enterobacterial common antigen biosynthesis restore outer membrane barrier function in Escherichia coli tol-pal mutants.,Molecular Microbiology

当前位置： X-MOL 学术 › Mol. Microbiol. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Mutations in enterobacterial common antigen biosynthesis restore outer membrane barrier function in Escherichia coli tol-pal mutants.
Molecular Microbiology ( IF 2.6 ) Pub Date : 2020-08-18 , DOI: 10.1111/mmi.14590
Xiang'Er Jiang ₁ , Wee Boon Tan ₂ , Rahul Shrivastava ₁ , Deborah Chwee San Seow ₃ , Swaine Lin Chen _{4,

5} , Xue Li Guan ₃ , Shu-Sin Chng _{1,

2}

Affiliation

The outer membrane (OM) is an essential component of the Gram‐negative bacterial envelope that protects the cells against external threats. To maintain a functional OM, cells require distinct mechanisms to ensure balance of proteins and lipids in the membrane. Mutations in OM biogenesis and/or homeostasis pathways often result in permeability defects, but how molecular changes in the OM affect barrier function is unclear. Here, we seek potential mechanism(s) that can alleviate permeability defects in Escherichia coli cells lacking the Tol‐Pal complex, which accumulate excess PLs in the OM. We identify mutations in enterobacterial common antigen (ECA) biosynthesis that re‐establish OM barrier function against large hydrophilic molecules, yet did not restore lipid homeostasis. Furthermore, we demonstrate that build‐up of biosynthetic intermediates, but not loss of ECA itself, contributes to the rescue. This suppression of OM phenotypes is unrelated to known effects that accumulation of ECA intermediates have on the cell wall. Finally, we reveal that an unusual diacylglycerol pyrophosphoryl‐linked lipid species also accumulates in ECA mutants, and might play a role in the rescue phenotype. Our work provides insights into how OM barrier function can be restored independent of lipid homeostasis, and highlights previously unappreciated effects of ECA‐related species in OM biology.

中文翻译：

肠道细菌共同抗原生物合成中的突变恢复了大肠杆菌 tol-pal 突变体的外膜屏障功能。

外膜 (OM) 是革兰氏阴性细菌包膜的重要组成部分，可保护细胞免受外部威胁。为了维持功能性 OM，细胞需要不同的机制来确保膜中蛋白质和脂质的平衡。OM 生物发生和/或稳态途径的突变通常会导致渗透性缺陷，但 OM 中的分子变化如何影响屏障功能尚不清楚。在这里，我们寻找可以减轻大肠杆菌渗透性缺陷的潜在机制缺乏 Tol-Pal 复合物的细胞会在 OM 中积累过量的 PL。我们鉴定了肠杆菌共同抗原 (ECA) 生物合成中的突变，这些突变重新建立了针对大亲水分子的 OM 屏障功能，但并未恢复脂质稳态。此外，我们证明了生物合成中间体的积累，而不是 ECA 本身的损失，有助于拯救。这种对 OM 表型的抑制与 ECA 中间体积累对细胞壁的已知影响无关。最后，我们揭示了一种不寻常的二酰基甘油焦磷酰基连接的脂质物质也在 ECA 突变体中积累，并且可能在拯救表型中发挥作用。我们的工作提供了关于如何在不依赖脂质稳态的情况下恢复 OM 屏障功能的见解，

更新日期：2020-08-18

点击分享查看原文

点击收藏

阅读更多本刊最新论文本刊介绍/投稿指南11