Evidence map›Paper›PMID 22159033›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Actin disassembly clock determines shape and speed of lamellipodial fragments.

Noa Ofer, Alexander Mogilner, Kinneret Keren

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing 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

47 citing papers in PubMed.

  1. Article
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  5. Length control emerges from cytoskeletal network geometry.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  6. Article
  7. Length control emerges from cytoskeletal network geometry.bioRxiv : the preprint server for biology · 2023
    Article
  8. Article
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  15. Article
  16. Overview of CaExploration of targeted anti-tumor therapy · 2021
    Review
  17. Stick-slip model for actin-driven cell protrusions, cell polarization, and crawling.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

Noa OferDepartment of Physics, Technion-Israel Institute of Technology, Haifa 32000, Israel.
Alexander Mogilner
Kinneret Keren

Funding

Modeling mitotic spindle assemblyR01GM068952 · NIGMS · UNIVERSITY OF CALIFORNIA DAVIS · PI MOGILNER, ALEXANDER · 2003 to 2014
$4.4M
NIGMS NIH HHS GM068952NIGMS NIH HHS R01 GM068952
6 · The paper itself

Abstract

A central challenge in motility research is to quantitatively understand how numerous molecular building blocks self-organize to achieve coherent shape and movement on cellular scales. A classic example of such self-organization is lamellipodial motility in which forward translocation is driven by a treadmilling actin network. Actin polymerization has been shown to be mechanically restrained by membrane tension in the lamellipodium. However, it remains unclear how membrane tension is determined, what is responsible for retraction and shaping of the rear boundary, and overall how actin-driven protrusion at the front is coordinated with retraction at the rear. To answer these questions, we utilize lamellipodial fragments from fish epithelial keratocytes which lack a cell body but retain the ability to crawl. The absence of the voluminous cell body in fragments simplifies the relation between lamellipodial geometry and cytoskeletal dynamics. We find that shape and speed are highly correlated over time within individual fragments, whereby faster crawling is accompanied by larger front-to-rear lamellipodial length. Furthermore, we find that the actin network density decays exponentially from front-to-rear indicating a constant net disassembly rate. These findings lead us to a simple hypothesis of a disassembly clock mechanism in which rear position is determined by where the actin network has disassembled enough for membrane tension to crush it and haul it forward. This model allows us to directly relate membrane tension with actin assembly and disassembly dynamics and elucidate the role of the cell membrane as a global mechanical regulator which coordinates protrusion and retraction.

Indexed as

ActinsAnimalsCell MembraneCell MovementCichlidsCytoskeletonEpithelial CellsFishesKeratinocytesMicroscopy, FluorescenceMicroscopy, Phase-ContrastModels, StatisticalMyosinsPseudopodiaActinsMyosins

Identifiers

PMID22159033
PMCPMC3251093

What OpenQuestion holds

Textmetadata
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.