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Mutations in enterobacterial common antigen biosynthesis restore outer membrane barrier function in Escherichia coli tol‐pal mutants
Author(s) -
Jiang Xiang’Er,
Tan Wee Boon,
Shrivastava Rahul,
Seow Deborah Chwee San,
Chen Swaine Lin,
Guan Xue Li,
Chng ShuSin
Publication year - 2020
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.14590
Subject(s) - biogenesis , biology , bacterial outer membrane , mutant , diacylglycerol kinase , cell envelope , escherichia coli , microbiology and biotechnology , barrier function , lipid a , secretion , biosynthesis , phenotype , function (biology) , biochemistry , genetics , bacteria , gene , signal transduction , protein kinase c
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.