Evidence map›Paper›PMID 21831921›Full record

ArticleDevelopment (Cambridge, England)2011

Cell cycle arrest in node cells governs ciliogenesis at the node to break left-right symmetry.

Yoshihiro Komatsu, Vesa Kaartinen, Yuji Mishina

Erratum issuedAbstract read
In one paragraph

Article in Development (Cambridge, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Disruption of distal appendage protein CEP164 causes skeletal malformation in mice.Biochemical and biophysical research communications · 2024
    Article
  2. Review
  3. Agonists of prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Article
  5. Article
  6. Primary Cilia Formation Does Not Rely on WNT/β-Catenin Signaling.Frontiers in cell and developmental biology · 2021
    Article
  7. Article
  8. Article
  9. TGF-β Family Signaling in Early Vertebrate Development.Cold Spring Harbor perspectives in biology · 2018
    Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. The type I BMP receptor ACVR1/ALK2 is required for chondrogenesis during development.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2015
    Article
  16. Article
  17. Review
  18. Review
  19. Review
  20. Left-right asymmetry: lessons from Cancún.Development (Cambridge, England) · 2013
    Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Yoshihiro KomatsuDepartment of Biologic and Materials Sciences, School of Dentistry, University of Michigan, 1011 North University Avenue, Ann Arbor, MI 48109-1078, USA.
Vesa Kaartinen
Yuji Mishina
University of Michigan–Ann Arbor · US

Funding

THE ROLE OF TGF-BETA3 IN PALATOGENESISR01DE013085 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAARTINEN, VESA M · 2001 to 2014
$5.4M
Molecular pathogenesis of craniosynostosis caused by enhanced BMP signalingR01DE020843 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MISHINA, YUJI · 2010 to 2019
$4.9M
Genetics Of Morphogenetic Mechanism During Mouse DevelopZ01ES071003 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI MISHINA, YUJI · 1998 to 2008
$4.3M
Activin Receptor-Like Kinase-2 in Cardiac MorphogenesisR01HL074862 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAARTINEN, VESA M · 2004 to 2011
$2.6M
Role of BMP signaling for chondrogenic fate determination in neural crest cellsK99DE021054 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KOMATSU, YOSHIHIRO · 2010 to 2011
$265k
Intramural NIH HHS Z01 ES071003NHLBI NIH HHS R01 HL074862NHLBI NIH HHS R01HL074862NIDCR NIH HHS K99 DE021054NIDCR NIH HHS K99DE021054NIDCR NIH HHS R01 DE013085NIDCR NIH HHS R01DE013085NIDCR NIH HHS R01 DE020843NIDCR NIH HHS R01DE020843NIEHS NIH HHS ES071003-11
6 · The paper itself

Abstract

Cilia at the node generate a leftward fluid flow that breaks left-right symmetry. However, the molecular mechanisms that regulate ciliogenesis at the node are largely unknown. Here, we show that the epiblast-specific deletion of the gene encoding the BMP type 1 receptor (Acvr1) compromised development of nodal cilia, which results in defects in leftward fluid flow and, thus, abnormalities in left-right patterning. Acvr1 deficiency in mouse embryonic fibroblasts (MEFs) resulted in severe defects in their quiescence-induced primary cilia. Although the induction of quiescence in wild-type MEFs leads to an increase in the level of the cyclin-dependent kinase inhibitor p27(Kip1) and to rapid p27(Kip1) phosphorylation on Ser(10), MEFs deficient in Acvr1 show a reduction in both p27(Kip1) protein levels and in p27(Kip1) Ser(10) phosphorylation. The observed defects in cilium development were rescued by the introduction of p27(Kip1) into Acvr1-deficient MEFs, implying that BMP signaling positively controls p27(Kip1) stability in the G0 phase via p27(Kip1) Ser(10) phosphorylation, which is a prerequisite for induction of primary cilia. Importantly, in control embryos, p27(Kip1) protein is clearly present and strongly phosphorylated on Ser(10) in cells on the quiescent ventral surface of the node. By contrast, the corresponding cells in the node of Acvr1 mutant embryos were proliferative and showed a dramatic attenuation in both p27(Kip1) protein levels and phosphorylation on Ser(10). Our data suggest that cell quiescence controlled by BMP signaling via ACVR1 is required for transient formation of nodal cilia, and provide insight into the fundamental question of how the node represents the mechanistic `node' that regulates the development of left-right symmetry in vertebrates.

Indexed as

Activin Receptors, Type IAnimalsBody PatterningBone Morphogenetic ProteinsCell CycleCells, CulturedCiliaEmbryo, MammalianFibroblastsMiceMice, KnockoutModels, BiologicalOrganizers, EmbryonicSignal TransductionActivin Receptors, Type IAcvr1 protein, mouseBone Morphogenetic Proteins

Identifiers

PMID21831921
PMCPMC3160088
OpenAlexW2163034747

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.