Evidence map›Paper›PMID 18434420›Full record

ArticleDevelopment (Cambridge, England)2008

Progressive myopathy and defects in the maintenance of myotendinous junctions in mice that lack talin 1 in skeletal muscle.

Francesco J Conti, Amanda Felder, Sue Monkley, Martin Schwander, Malcolm R Wood, Richard Lieber, David Critchley, Ulrich Müller

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2008. 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
2.1field-weighted citation impact, top 15% 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, 51 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. LanB1 Cooperates With Kon-Tiki During Embryonic Muscle Migration inFrontiers in cell and developmental biology · 2021
    Article
  6. Article
  7. Using tools in mechanobiology to repair tendons.Current tissue microenvironment reports · 2020
    Article
  8. Article
  9. Article
  10. Article
  11. Overview of the Muscle Cytoskeleton.Comprehensive Physiology · 2017
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Talins and kindlins: partners in integrin-mediated adhesion.Nature reviews. Molecular cell biology · 2013
    Review
  17. Article
  18. Article
  19. Mice carrying a complete deletion of the talin2 coding sequence are viable and fertile.Biochemical and biophysical research communications · 2012
    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

8 authors at 3 institutions in 2 countries.

Francesco J ContiThe Scripps Research Institute, Department of Cell Biology and Institute of Childhood and Neglected Disease, La Jolla, CA 92037, USA.
Amanda Felder
Sue Monkley
Martin Schwander
Malcolm R Wood
Richard Lieber
David Critchley
Ulrich Müller
Scripps Research Institute · USLa Jolla Bioengineering Institute · USUniversity of Leicester · GB

Funding

Cell Adhesion Molecules in CNS DevelopmentR01NS046456 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI MUELLER, ULRICH · 2004 to 2013
$4.4M
Skeletal Muscle Injury: Mechanism Prevention &TreatmentR01AR040050 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIEBER, RICHARD L · 1989 to 2007
$1.6M
NIAMS NIH HHS AR40050NINDS NIH HHS NS046456NINDS NIH HHS R01 NS046456Wellcome Trust 077532
6 · The paper itself

Abstract

The development and function of skeletal muscle depend on molecules that connect the muscle fiber cytoskeleton to the extracellular matrix (ECM). beta1 integrins are ECM receptors in skeletal muscle, and mutations that affect the alpha7beta1 integrin cause myopathy in humans. In mice, beta1 integrins control myoblast fusion, the assembly of the muscle fiber cytoskeleton, and the maintenance of myotendinous junctions (MTJs). The effector molecules that mediate beta1 integrin functions in muscle are not known. Previous studies have shown that talin 1 controls the force-dependent assembly of integrin adhesion complexes and regulates the affinity of integrins for ligands. Here we show that talin 1 is essential in skeletal muscle for the maintenance of integrin attachment sites at MTJs. Mice with a skeletal muscle-specific ablation of the talin 1 gene suffer from a progressive myopathy. Surprisingly, myoblast fusion and the assembly of integrin-containing adhesion complexes at costameres and MTJs advance normally in the mutants. However, with progressive ageing, the muscle fiber cytoskeleton detaches from MTJs. Mechanical measurements on isolated muscles show defects in the ability of talin 1-deficient muscle to generate force. Collectively, our findings show that talin 1 is essential for providing mechanical stability to integrin-dependent adhesion complexes at MTJs, which is crucial for optimal force generation by skeletal muscle.

Indexed as

Actin CytoskeletonAnimalsBlotting, WesternExtracellular MatrixImmunohistochemistryIntegrin beta1IntegrinsMiceMice, KnockoutMicroscopy, ElectronMicroscopy, FluorescenceModels, GeneticMuscle, SkeletalMuscular DiseasesMuscular DystrophiesReverse Transcriptase Polymerase Chain ReactionIntegrin beta1IntegrinsTalinTln1 protein, mouseTLN2 protein, mouse

Identifiers

PMID18434420
PMCPMC2562324
OpenAlexW2010388546

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.