Evidence map›Paper›PMID 36701201›Full record

ArticleThe Biochemical journal2023

Interaction of the periplasmic chaperone SurA with the inner membrane protein secretion (SEC) machinery.

Luca A Troman, Sara Alvira, Bertram Daum, Vicki A M Gold, Ian Collinson

Open access · hybridAbstract read
In one paragraph

Article in The Biochemical journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
2.5field-weighted citation impact, top 11% of its field
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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. YidC fromBiomolecules · 2023
    Article
  6. 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

5 authors at 2 institutions in 1 country.

Luca A TromanSchool of Biochemistry, University of Bristol, Bristol BS8 1TD, U.K.ORCID 0000-0003-3494-4192
Sara AlviraSchool of Biochemistry, University of Bristol, Bristol BS8 1TD, U.K.
Bertram DaumLiving Systems Institute, University of Exeter, Exeter, U.K.
Vicki A M GoldLiving Systems Institute, University of Exeter, Exeter, U.K.ORCID 0000-0002-6908-0745
Ian CollinsonSchool of Biochemistry, University of Bristol, Bristol BS8 1TD, U.K.ORCID 0000-0002-3931-0503
University of Bristol · GBUniversity of Exeter · GB

Funding

Biotechnology and Biological Sciences Research Council BB/J014400/1Biotechnology and Biological Sciences Research Council BB/M009122/1Biotechnology and Biological Sciences Research Council BB/R000484/1Biotechnology and Biological Sciences Research Council BB/R008639/1Biotechnology and Biological Sciences Research Council BB/S008349/1Wellcome Trust 202904/Z/16/ZWellcome Trust 204813/Z/16/ZWellcome Trust 206181/Z/17/Z
6 · The paper itself

Abstract

Gram-negative bacteria are surrounded by two protein-rich membranes with a peptidoglycan layer sandwiched between them. Together they form the envelope (or cell wall), crucial for energy production, lipid biosynthesis, structural integrity, and for protection against physical and chemical environmental challenges. To achieve envelope biogenesis, periplasmic and outer-membrane proteins (OMPs) must be transported from the cytosol and through the inner-membrane, via the ubiquitous SecYEG protein-channel. Emergent proteins either fold in the periplasm or cross the peptidoglycan (PG) layer towards the outer-membrane for insertion through the β-barrel assembly machinery (BAM). Trafficking of hydrophobic proteins through the periplasm is particularly treacherous given the high protein density and the absence of energy (ATP or chemiosmotic potential). Numerous molecular chaperones assist in the prevention and recovery from aggregation, and of these SurA is known to interact with BAM, facilitating delivery to the outer-membrane. However, it is unclear how proteins emerging from the Sec-machinery are received and protected from aggregation and proteolysis prior to an interaction with SurA. Through biochemical analysis and electron microscopy we demonstrate the binding capabilities of the unoccupied and substrate-engaged SurA to the inner-membrane translocation machinery complex of SecYEG-SecDF-YidC - aka the holo-translocon (HTL). Supported by AlphaFold predictions, we suggest a role for periplasmic domains of SecDF in chaperone recruitment to the protein translocation exit site in SecYEG. We propose that this immediate interaction with the enlisted chaperone helps to prevent aggregation and degradation of nascent envelope proteins, facilitating their safe passage to the periplasm and outer-membrane.

Indexed as

Escherichia coli ProteinsPeriplasmBacterial Outer Membrane ProteinsCarrier ProteinsEscherichia coliMembrane ProteinsMembrane Transport ProteinsMolecular ChaperonesPeptidoglycanPeptidylprolyl IsomeraseBacterial Outer Membrane ProteinsCarrier ProteinsEscherichia coli ProteinsMembrane ProteinsMembrane Transport ProteinsMolecular ChaperonesPeptidoglycanPeptidylprolyl IsomeraseSurA protein, E coliYIDC protein, E colibacterial envelopebiogenesischaperonesprotein secretionSec transloconSurA

Identifiers

PMID36701201
PMCPMC9987972
OpenAlexW4318071688

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.