Evidence map›Paper›PMID 20543839›Full record

ArticleNature cell biology2010

Myosin II isoforms identify distinct functional modules that support integrity of the epithelial zonula adherens.

Michael Smutny, Hayley L Cox, Joanne M Leerberg, Eva M Kovacs, Mary Anne Conti, Charles Ferguson, Nicholas A Hamilton, Robert G Parton, Robert S Adelstein, Alpha S Yap

Open access · greenAbstract read
In one paragraph

Article in Nature cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 193 papers.

0numbers the graph read from it
0cells of the map it votes in
193citing papers in PubMed
15.1field-weighted citation impact, top 1% 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

193 citing papers in PubMed, 327 citations in OpenAlex.

  1. International journal of molecular sciences · 2026
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  12. Non-Muscle Myosin II A: Friend or Foe in Cancer?International journal of molecular sciences · 2024
    Review
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133 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Michael SmutnyInstitute for Molecular Bioscience, Division of Molecular Cell Biology, The University of Queensland, St. Lucia, Brisbane, Queensland 4072, Australia.
Hayley L Cox
Joanne M Leerberg
Eva M Kovacs
Mary Anne Conti
Charles Ferguson
Nicholas A Hamilton
Robert G Parton
Robert S Adelstein
Alpha S Yap
University of Queensland · AUNational Heart Lung and Blood Institute · US

Funding

In Vivo Function of Nonmuscle Myosin II-AZIAHL004218 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ADELSTEIN, ROBERT · 2009 to 2019
$5.1M
In Vivo Function of Nonmuscle Myosin II-AZ01HL004218 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI ADELSTEIN, ROBERT · 1991 to 2008
$826k
Austrian Science Fund FWF J 2621Intramural NIH HHS Z01 HL004218Intramural NIH HHS Z99 HL999999
6 · The paper itself

Abstract

Classic cadherin receptors cooperate with regulators of the actin cytoskeleton to control tissue organization in health and disease. At the apical junctions of epithelial cells, the cadherin ring of the zonula adherens (ZA) couples with a contiguous ring of actin filaments to support morphogenetic processes such as tissue integration and cellular morphology. However, the molecular mechanisms that coordinate adhesion and cytoskeleton at these junctions are poorly understood. Previously we identified non-muscle myosin II as a target of Rho signalling that supports cadherin junctions in mammalian epithelial cells. Myosin II has various cellular functions, which are increasingly attributable to the specific biophysical properties and regulation of its different isoforms. Here we report that myosin II isoforms have distinct and necessary roles at cadherin junctions. Although two of the three mammalian myosin II isoforms are found at the ZA, their localization is regulated by different upstream signalling pathways. Junctional localization of myosin IIA required E-cadherin adhesion, Rho/ROCK and myosin light-chain kinase, whereas junctional myosin IIB depended on Rap1. Further, these myosin II isoforms support E-cadherin junction integrity by different mechanisms. Myosin IIA RNA-mediated interference (RNAi) selectively perturbed the accumulation of E-cadherin in the apical ZA, decreased cadherin homophilic adhesion and disrupted cadherin clustering. In contrast, myosin IIB RNAi decreased filament content, altered dynamics, and increased the lateral movement of the perijunctional actin ring. Myosin IIA and IIB therefore identify two distinct functional modules, with different upstream signals that control junctional localization, and distinct functional effects. We propose that these two isoform-based modules cooperate to coordinate adhesion receptor and F-actin organization to form apical cadherin junctions.

Indexed as

Adherens JunctionsCadherinsCell Line, TumorHumansModels, BiologicalNonmuscle Myosin Type IIANonmuscle Myosin Type IIBCadherinsNonmuscle Myosin Type IIANonmuscle Myosin Type IIB

Identifiers

PMID20543839
PMCPMC3428211
OpenAlexW2060545109

What OpenQuestion holds

Textmetadata
LicenceTDM
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.