Dead‐end intermediates in the enterobacterial common antigen pathway induce morphological defects in Escherichia coli by competing for undecaprenyl phosphate

Summary Bacterial morphology is determined primarily by the architecture of the peptidoglycan ( PG ) cell wall, a mesh‐like layer that encases the cell. To identify novel mechanisms that create or maintain cell shape in E scherichia coli , we used flow cytometry to screen a transposon insertion library and identified a wec E mutant that altered cell shape, causing cells to filament and swell. WecE is a sugar aminotransferase involved in the biosynthesis of enterobacterial common antigen ( ECA ), a non‐essential outer membrane glycolipid of the E nterobacteriaceae . Loss of wec E interrupts biosynthesis of ECA and causes the accumulation of the undecaprenyl pyrophosphate‐linked intermediate ECA ‐lipid II . The wec E shape defects were reversed by: (i) preventing initiation of ECA biosynthesis, (ii) increasing the synthesis of the lipid carrier undecaprenyl phosphate ( U nd‐ P ), (iii) diverting U nd‐ P to PG synthesis or (iv) promoting U nd‐ P recycling. The results argue that the buildup of ECA ‐lipid II sequesters part of the pool of U nd‐ P , which, in turn, adversely affects PG synthesis. The data strongly suggest there is competition for a common pool of U nd‐ P , whose proper distribution to alternate metabolic pathways is required to maintain normal cell shape in E . coli .