Evidence map›Paper›PMID 35389747›Full record

ArticleMolecular biology of the cell2022

Load adaptation by endocytic actin networks.

Charlotte Kaplan, Sam J Kenny, Xuyan Chen, Johannes Schöneberg, Ewa Sitarska, Alba Diz-Muñoz, Matthew Akamatsu, Ke Xu, David G Drubin

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

17 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Endocytic myosin-1 is a force-insensitive, power-generating motor.bioRxiv : the preprint server for biology · 2023
    Article
  10. Article
  11. Article
  12. Biochemical and mechanical regulation of actin dynamics.Nature reviews. Molecular cell biology · 2022
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
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

9 authors at 4 institutions in 2 countries.

Charlotte KaplanDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720-3220.
Sam J KennyDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720-3220.
Xuyan ChenDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720-3220.
Johannes SchönebergDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720-3220.
Ewa SitarskaCell Biology and Biophysics Unit, European Molecular Biology Laboratory Heidelberg, 69117 Heidelberg, Germany.
Alba Diz-MuñozCell Biology and Biophysics Unit, European Molecular Biology Laboratory Heidelberg, 69117 Heidelberg, Germany.
Matthew AkamatsuDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720-3220.
Ke XuDepartment of Chemistry, University of California, Berkeley, Berkeley, CA 94720-3220.
David G DrubinDepartment of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720-3220.
University of California, Berkeley · USEuropean Molecular Biology Laboratory · DEChan Zuckerberg Initiative (United States) · USUniversity of California, San Diego · US

Funding

Nikon confocal system for improved spatio-dynamic analysis of endocytic trafficking eventsR35GM118149 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI DAVID G DRUBIN · 2016 to 2026
$12.0M
Molecular and biophysical mechanism of plasma membrane internalization during nonclathrin endocytosisR00GM132551 · NIGMS · UNIVERSITY OF WASHINGTON · PI AKAMATSU, MATTHEW SATARO · 2023 to 2025
$747k
Molecular and biophysical mechanism of plasma membrane internalization during nonclathrin endocytosisK99GM132551 · NIGMS · UNIVERSITY OF CALIFORNIA BERKELEY · PI AKAMATSU, MATTHEW SATARO · 2019 to 2020
$194k
NIGMS NIH HHS K99 GM132551NIGMS NIH HHS R00 GM132551NIGMS NIH HHS R35 GM118149
6 · The paper itself

Abstract

Clathrin-mediated endocytosis (CME) robustness under elevated membrane tension is maintained by actin assembly-mediated force generation. However, whether more actin assembles at endocytic sites in response to increased load has not previously been investigated. Here actin network ultrastructure at CME sites was examined under low and high membrane tension. Actin and N-WASP spatial organization indicate that actin polymerization initiates at the base of clathrin-coated pits and that the network then grows away from the plasma membrane. Actin network height at individual CME sites was not coupled to coat shape, raising the possibility that local differences in mechanical load feed back on assembly. By manipulating membrane tension and Arp2/3 complex activity, we tested the hypothesis that actin assembly at CME sites increases in response to elevated load. Indeed, in response to elevated membrane tension, actin grew higher, resulting in greater coverage of the clathrin coat, and CME slowed. When membrane tension was elevated and the Arp2/3 complex was inhibited, shallow clathrin-coated pits accumulated, indicating that this adaptive mechanism is especially crucial for coat curvature generation. We propose that actin assembly increases in response to increased load to ensure CME robustness over a range of plasma membrane tensions.

Indexed as

ActinsClathrinActin-Related Protein 2-3 ComplexCell MembraneEndocytosisActin-Related Protein 2-3 ComplexActinsClathrin

Identifiers

PMID35389747
PMCPMC9265150
OpenAlexW4226073694

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.