Evidence map›Paper›PMID 41044071›Full record

ArticleNature communications2025

Molecular insights into how the motions of the β-barrel and POTRA domains of BamA are coupled for efficient function.

Naemi Csoma, Jonathan M Machin, James M Whitehouse, Raquel Rodrìguez-Alonso, Monika Olejnik, Adam K Cahill, Seung-Hyun Cho, Till F Schäberle, Bogdan I Iorga, Neil A Ranson and 3 more

Abstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Naemi Csoma *WELBIO Department, WEL Research Institute, Wavre, Belgium.ORCID http://orcid.org/0000-0002-2858-5771
Jonathan M Machin *Astbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
James M Whitehouse *Astbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
Raquel Rodrìguez-AlonsoWELBIO Department, WEL Research Institute, Wavre, Belgium.ORCID http://orcid.org/0000-0001-5548-6819
Monika OlejnikAstbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.
Adam K CahillAstbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.ORCID http://orcid.org/0009-0001-9074-7719
Seung-Hyun ChoWELBIO Department, WEL Research Institute, Wavre, Belgium.ORCID http://orcid.org/0000-0002-5548-4239
Till F SchäberleInstitute for Insect Biotechnology, Justus-Liebig-University Giessen, Giessen, Germany.ORCID http://orcid.org/0000-0001-9947-8079
Bogdan I Iorgade Duve Institute, Université catholique de Louvain (UCLouvain), Brussels, Belgium.ORCID http://orcid.org/0000-0003-0392-1350
Neil A RansonAstbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK.ORCID http://orcid.org/0000-0002-3640-5275
Sheena E RadfordAstbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK. s.e.radford@leeds.ac.uk.ORCID http://orcid.org/0000-0002-3079-8039
Antonio N CalabreseAstbury Centre for Structural Molecular Biology, School of Molecular and Cellular Biology, Faculty of Biological Sciences, University of Leeds, Leeds, UK. a.calabrese@leeds.ac.uk.ORCID http://orcid.org/0000-0003-2437-7761
Jean-François ColletWELBIO Department, WEL Research Institute, Wavre, Belgium. jfcollet@uclouvain.be.ORCID http://orcid.org/0000-0001-8069-7036

Funding

Wellcome Trust 221524
6 · The paper itself

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.

Indexed as

Bacterial Outer Membrane ProteinsEscherichia coliEscherichia coli ProteinsCryoelectron MicroscopyModels, MolecularMutationProtein DomainsBacterial Outer Membrane ProteinsBamA protein, E coliEscherichia coli Proteins

Identifiers

PMID41044071
PMCPMC12494951

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.