A central role for PBP2 in the activation of peptidoglycan polymerization by the bacterial cell elongation machinery

Cell elongation in rod-shaped bacteria is mediated by the Rod system, a conserved morphogenic complex that spatially controls cell wall assembly by the glycan polymerase RodA and crosslinking enzyme PBP2. Using Escherichia coli as a model system, we identified a PBP2 variant that promotes Rod system...

Full description

Saved in:
Bibliographic Details
Published inPLoS genetics Vol. 14; no. 10; p. e1007726
Main Authors Rohs, Patricia D A, Buss, Jackson, Sim, Sue I, Squyres, Georgia R, Srisuknimit, Veerasak, Smith, Mandy, Cho, Hongbaek, Sjodt, Megan, Kruse, Andrew C, Garner, Ethan C, Walker, Suzanne, Kahne, Daniel E, Bernhardt, Thomas G
Format Journal Article
LanguageEnglish
Published United States Public Library of Science 01.10.2018
Public Library of Science (PLoS)
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Cell elongation in rod-shaped bacteria is mediated by the Rod system, a conserved morphogenic complex that spatially controls cell wall assembly by the glycan polymerase RodA and crosslinking enzyme PBP2. Using Escherichia coli as a model system, we identified a PBP2 variant that promotes Rod system function when essential accessory components of the machinery are inactivated. This PBP2 variant hyperactivates cell wall synthesis in vivo and stimulates the activity of RodA-PBP2 complexes in vitro. Cells with the activated synthase also exhibited enhanced polymerization of the actin-like MreB component of the Rod system. Our results define an activation pathway governing Rod system function in which PBP2 conformation plays a central role in stimulating both glycan polymerization by its partner RodA and the formation of cytoskeletal filaments of MreB to orient cell wall assembly. In light of these results, previously isolated mutations that activate cytokinesis suggest that an analogous pathway may also control cell wall synthesis by the division machinery.
Bibliography:new_version
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
The authors have declared that no competing interests exist.
ISSN:1553-7404
1553-7390
1553-7404
DOI:10.1371/journal.pgen.1007726