Evidence map›Paper›PMID 35489383›Full record

ArticleJournal of molecular biology2022

Topology of the SecA ATPase Bound to Large Unilamellar Vesicles.

Guillaume Roussel, Eric Lindner, Stephen H White

Open access · hybridAbstract read
In one paragraph

Article in Journal of molecular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. SecYEG-mediated translocation in a model synthetic cell.Synthetic biology (Oxford, England) · 2024
    Article
  3. Article
  4. Review
  5. 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

3 authors at 1 institution in 1 country.

Guillaume RousselDepartment of Physiology and Biophysics, University of California, Irvine, Irvine, CA 92697-4560, United States.
Eric LindnerDepartment of Physiology and Biophysics, University of California, Irvine, Irvine, CA 92697-4560, United States.
Stephen H WhiteDepartment of Physiology and Biophysics, University of California, Irvine, Irvine, CA 92697-4560, United States. Electronic address: stephen.white@uci.edu.
University of California, Irvine · US

Funding

Membrane Protein Folding and AssemblyR01GM074637 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI WHITE, STEPHEN H. · 2006 to 2020
$4.5M
Membrane Protein Folding and AssemblyR35GM139652 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI WHITE, STEPHEN H. · 2021 to 2025
$2.0M
NIGMS NIH HHS R01 GM074637NIGMS NIH HHS R35 GM139652
6 · The paper itself

Abstract

The soluble cytoplasmic ATPase motor protein SecA powers protein transport across the Escherichia coli inner membrane via the SecYEG translocon. Although dimeric in solution, SecA associates monomerically with SecYEG during secretion according to several crystallographic and cryo-EM structural studies. The steps SecA follows from its dimeric cytoplasmic state to its active SecYEG monomeric state are largely unknown. We have previously shown that dimeric SecA in solution dissociates into monomers upon electrostatic binding to negatively charged lipid vesicles formed from E. coli lipids. Here we address the question of the disposition of SecA on the membrane prior to binding to membrane embedded SecYEG. We mutated to cysteine, one at a time, 25 surface-exposed residues of a Cys-free SecA. To each of these we covalently linked the polarity-sensitive fluorophore NBD whose intensity and fluorescence wavelength-shift change upon vesicle binding report on the the local membrane polarity. We established from these measurements the disposition of SecA bound to the membrane in the absence of SecYEG. Our results confirmed that SecA is anchored in the membrane interface primarily by the positive charges of the N terminus domain. But we found that a region of the nucleotide binding domain II is also important for binding. Both domains are rich in positively charged residues, consistent with electrostatic interactions playing the major role in membrane binding. Selective replacement of positively charged residues in these domains with alanine resulted in weaker binding to the membrane, which allowed us to quantitate the relative importance of the domains in stabilizing SecA on membranes. Fluorescence quenchers inside the vesicles had little effect on NBD fluorescence, indicating that SecA does not penetrate significantly across the membrane. Overall, the topology of SecA on the membrane is consistent with the conformation of SecA observed in crystallographic and cryo-EM structures of SecA-SecYEG complexes, suggesting that SecA can switch between the membrane-associated and the translocon-associated states without significant changes in conformation.

Indexed as

Escherichia coliEscherichia coli ProteinsSecA ProteinsUnilamellar LiposomesCryoelectron MicroscopyProtein BindingProtein DomainsProtein MultimerizationProtein TransportSEC Translocation ChannelsEscherichia coli ProteinsSecA protein, E coliSecA ProteinsSEC Translocation ChannelsUnilamellar Liposomesfluorescencemembrane protein topologyNBD-labelingpartitioning free energyperipheral membrane protein

Identifiers

PMID35489383
PMCPMC10085631
OpenAlexW4225278551

What OpenQuestion holds

Textmetadata
LicenceTDM
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.