Evidence map›Paper›PMID 18390606›Full record

ArticleBiophysical journal2008

Performance of a population of independent filaments in lamellipodial protrusion.

Thomas E Schaus, Gary G Borisy

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Power transduction of actin filaments ratcheting in vitro against a load.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Mathematical modeling of eukaryotic cell migration: insights beyond experiments.Annual review of cell and developmental biology · 2013
    Review
  15. Article
  16. Mesoscopic model of actin-based propulsion.PLoS computational biology · 2012
    Article
  17. Actin disassembly clock determines shape and speed of lamellipodial fragments.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  18. Article
  19. Cell motility: the integrating role of the plasma membrane.European biophysics journal : EBJ · 2011
    Review
  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

2 authors at 1 institution in 1 country.

Thomas E SchausDepartment of Cell and Molecular Biology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. tschaus@northwestern.edu
Gary G Borisy
Northwestern University · US

Funding

MECHANISM OF ACTIN-BASED CELL MOTILITYR01GM062431 · NIGMS · NORTHWESTERN UNIVERSITY · PI BORISY, GARY G · 2001 to 2004
$1.1M
NIGMS NIH HHS GM 62431NIGMS NIH HHS R01 GM062431
6 · The paper itself

Abstract

Actin polymerization is responsible for moving a wide variety of loads, from the protrusion of membrane-bound filopodia and lamellipodia of immune, cancer, and other motile cells, to the propulsion of some intracellular pathogens. A universal explanation of the forces and velocities generated by these systems has been hampered by a lack of understanding in how a population of independent filaments pushes these loads. Protrusion of a lamellipodium by the very filaments supporting the membrane load is thought to operate by the Brownian ratchet mechanism, with overall organization governed by the dendritic-nucleation/array-treadmilling model. We have incorporated these two models into a two-dimensional, stochastic computer model of lamellipodial protrusion, and studied how force and velocity generation varied under different assumptions. Performance is very sensitive to the extent to which the work of protrusion is shared among individual polymerization events within the filament population. Three identified mechanisms promote this "work-sharing": 1), Most systems, including lamellipodia, utilize a self-organizing distribution of filament-load distances which serves to decrease the effective size of a monomer and dramatically improve performance. 2), A flexible membrane allows for consistent performance over wide leading edges. 3), Finally, very flexible filaments are capable of sharing work very uniformly, and therefore, of near-perfect theoretical performance. Transient tethering to the lamellipodial membrane limits their efficacy, however, and mandates a minimum filament stiffness. Overall, we estimate lamellipodia to operate with 40-nm bending-length filaments and low characteristic tether forces. Modeled lamellipodia exhibit sigmoidal force-velocity relationships and share the work of protrusion only moderately well among filaments, performing at approximately one-half of theoretical force and velocity maximums. At this level of work-sharing, the natural monomer size is optimal for generating velocity.

Indexed as

Models, BiologicalModels, ChemicalActin CytoskeletonComputer SimulationMolecular Motor ProteinsPseudopodiaStress, MechanicalMolecular Motor Proteins

Identifiers

PMID18390606
PMCPMC2479583
OpenAlexW2017364338

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.