ArticlePLoS genetics2021
Genetic analysis of the septal peptidoglycan synthase FtsWI complex supports a conserved activation mechanism for SEDS-bPBP complexes.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- RodZ acts through MreBCD to activate the elongasome inJournal of bacteriology · 2026Article
- Altered regulation of septal peptidoglycan synthesis modulates β-lactam susceptibility in Pseudomonas aeruginosa.PLoS genetics · 2026Article
- Article
- Direct interaction between MreB and the RodA-PBP2 complex organizes lateral cell wall synthesis inmLife · 2026Article
- Control of cell division by anbioRxiv : the preprint server for biology · 2026Article
- Article
- Mechanistic Insights into the Antimicrobial Effect of Benzodioxane-Benzamides AgainstAntibiotics (Basel, Switzerland) · 2026Article
- Antibiotic-resistance mutations in penicillin-binding protein 2 from the ceftriaxone-resistantbioRxiv : the preprint server for biology · 2025Article
- Article
- Septal wall synthesis is sufficient to change ameba-like cells into uniform oval-shaped cells in Escherichia coli L-forms.Communications biology · 2024Article
- Article
- The divisome is a self-enhancing machine in Escherichia coli and Caulobacter crescentus.Nature communications · 2024Article
- Pbp4 provides transpeptidase activity to the FtsW-PbpB peptidoglycan synthase to drive cephalosporin resistance inAntimicrobial agents and chemotherapy · 2024Article
- Article
- Role of the antiparallel double-stranded filament form of FtsA in activating thebioRxiv : the preprint server for biology · 2024Article
- Structural insights into the activation of the divisome complex FtsWIQLB.Cell discovery · 2024Article
- Insights into the assembly and regulation of the bacterial divisome.Nature reviews. Microbiology · 2024Review
- Conformational changes in the essential E. coli septal cell wall synthesis complex suggest an activation mechanism.Nature communications · 2023Article
- Cryo-EM structure of the bacterial divisome core complex and antibiotic target FtsWIQBL.Nature microbiology · 2023Article
- Bacterial divisome protein FtsA forms curved antiparallel double filaments when binding to FtsN.Nature microbiology · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
SEDS family peptidoglycan (PG) glycosyltransferases, RodA and FtsW, require their cognate transpeptidases PBP2 and FtsI (class B penicillin binding proteins) to synthesize PG along the cell cylinder and at the septum, respectively. The activities of these SEDS-bPBPs complexes are tightly regulated to ensure proper cell elongation and division. In Escherichia coli FtsN switches FtsA and FtsQLB to the active forms that synergize to stimulate FtsWI, but the exact mechanism is not well understood. Previously, we isolated an activation mutation in ftsW (M269I) that allows cell division with reduced FtsN function. To try to understand the basis for activation we isolated additional substitutions at this position and found that only the original substitution produced an active mutant whereas drastic changes resulted in an inactive mutant. In another approach we isolated suppressors of an inactive FtsL mutant and obtained FtsWE289G and FtsIK211I and found they bypassed FtsN. Epistatic analysis of these mutations and others confirmed that the FtsN-triggered activation signal goes from FtsQLB to FtsI to FtsW. Mapping these mutations, as well as others affecting the activity of FtsWI, on the RodA-PBP2 structure revealed they are located at the interaction interface between the extracellular loop 4 (ECL4) of FtsW and the pedestal domain of FtsI (PBP3). This supports a model in which the interaction between the ECL4 of SEDS proteins and the pedestal domain of their cognate bPBPs plays a critical role in the activation mechanism.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.