Evidence map›Paper›PMID 1918159›Full record

ArticleThe Journal of cell biology1991

The structural basis for the intrinsic disorder of the actin filament: the "lateral slipping" model.

A Bremer, R C Millonig, R Sütterlin, A Engel, T D Pollard, U Aebi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Review
  3. Mechanism of actin filament nucleation.Biophysical journal · 2021
    Article
  4. Article
  5. Article
  6. Helical rotation of the diaphanous-related formin mDia1 generates actin filaments resistant to cofilin.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  7. Article
  8. Intermittent depolymerization of actin filaments is caused by photo-induced dimerization of actin protomers.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Actin-destabilizing factors disrupt filaments by means of a time reversal of polymerization.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Actin and the smooth muscle regulatory proteins: a structural perspective.Journal of muscle research and cell motility · 2000
    Review
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

A BremerM.E. Müller-Institute for High-Resolution Electron Microscopy at the Biocenter, University of Basel, Switzerland.
R C Millonig
R Sütterlin
A Engel
T D Pollard
U Aebi
University of Basel · CH

Funding

STRUCTURE/INTERACTIONS OF ACTINS &ACTIN-BINDING PROTEINR01GM035171 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI LATTMAN, EATON E · 1985 to 1995
–
NIGMS NIH HHS R01-GM35171
6 · The paper itself

Abstract

Three-dimensional (3-D) helical reconstructions computed from electron micrographs of negatively stained dispersed F-actin filaments invariably revealed two uninterrupted columns of mass forming the "backbone" of the double-helical filament. The contact between neighboring subunits along the thus defined two long-pitch helical strands was spatially conserved and of high mass density, while the intersubunit contact between them was of lower mass density and varied among reconstructions. In contrast, phalloidinstabilized F-actin filaments displayed higher and spatially more conserved mass density between the two long-pitch helical strands, suggesting that this bicyclic hepta-peptide toxin strengthens the intersubunit contact between the two strands. Consistent with this distinct intersubunit bonding pattern, the two long-pitch helical strands of unstabilized filaments were sometimes observed separated from each other over a distance of two to six subunits, suggesting that the intrastrand intersubunit contact is also physically stronger than the interstrand contact. The resolution of the filament reconstructions, extending to 2.5 nm axially and radially, enabled us to reproducibly "cut out" the F-actin subunit which measured 5.5 nm axially by 6.0 nm tangentially by 3.2 nm radially. The subunit is distinctly polar with a massive "base" pointing towards the "barbed" end of the filament, and a slender "tip" defining its "pointed" end (i.e., relative to the "arrowhead" pattern revealed after stoichiometric decoration of the filaments with myosin subfragment 1). Concavities running approximately parallel to the filament axis both on the inner and outer face of the subunit define a distinct cleft separating the subunit into two domains of similar size: an inner domain confined to radii less than or equal to 2.5-nm forms the uninterrupted backbone of the two long-pitch helical strands, and an outer domain placed at radii of 2-5-nm protrudes radially and thus predominantly contributes to the outer part of the massive base. Quantitative evaluation of successive crossover spacings along individual F-actin filaments revealed the deviations from the mean repeat to be compensatory, i.e., short crossovers frequently followed long ones and vice versa. The variable crossover spacings and diameter of the F-actin filament together with the local unraveling of the two long-pitch helical strands are explained in terms of varying amounts of compensatory "lateral slipping" of the two strands past each other roughly perpendicular to the filament axis. This intrinsic disorder of the actin filament may enable the actin moiety to play a more active role in actin-myosin-based force generation than merely act as a rigid passive cable as has hitherto been assumed.

Indexed as

ActinsAnimalsFourier AnalysisMicroscopy, ElectronModels, StructuralMusclesPhalloidineProtein ConformationRabbitsActinsPhalloidine

Identifiers

PMID1918159
PMCPMC2289171
OpenAlexW2014098520

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.