ArticleNature communications2025
Molecular insights into how the motions of the β-barrel and POTRA domains of BamA are coupled for efficient function.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- BamA as a next-generation antibacterial target: mechanistic insights, inhibitor landscape, and rational drug design strategies.RSC advances · 2026Review
- Monitoring Membrane Protein Folding Assisted by Insertases and Translocases Using AFM-Based Single-Molecule Force Spectroscopy.Chemical reviews · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
Abstract
The β-barrel assembly machinery (BAM) inserts β-barrel proteins into the outer membrane of Gram-negative bacteria, forming an essential permeability barrier. The core BAM component, BamA, is a β-barrel protein with an N-terminal periplasmic extension comprising five polypeptide transport-associated (POTRA) domains. Whilst BamA's structure is well characterised, it remains unclear how β-barrel and POTRA domain motions are coordinated. Using BamA variants with mutations in the hinge region between these two domains, we demonstrate that hinge flexibility is required for BAM function. Cryo-electron microscopy suggests that hinge rigidity impairs function by structurally decoupling these domains. A screen for spontaneous suppressors identified a mutation at position T434 in an extracellular loop of BamA, which has been previously shown to suppress BAM defects. Studying this variant provides insights into its function as a general rescue mechanism. Our findings underscore how BamA's sequence has been evolutionarily optimised for efficient function.
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Registered trials
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