Evidence map›Paper›PMID 29593116›Full record

ArticleOpen biology2018

TGFβ-facilitated optic fissure fusion and the role of bone morphogenetic protein antagonism.

Max D Knickmeyer, Juan L Mateo, Priska Eckert, Eleni Roussa, Belal Rahhal, Aimee Zuniga, Kerstin Krieglstein, Joachim Wittbrodt, Stephan Heermann

Open access · goldAbstract read
In one paragraph

Article in Open biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.9field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Holoprosencephaly and cyclopia inAnimal cells and systems · 2025
    Article
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  11. Review
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  13. Observational
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  18. Frontiers in cell and developmental biology · 2020
    Review
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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

9 authors at 3 institutions in 3 countries.

Max D KnickmeyerDepartment of Molecular Embryology, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg D-79104, Germany.
Juan L MateoDepartamento de Informática, Universidad de Oviedo, Jesús Arias de Velasco, Oviedo 33005, Spain.
Priska EckertDepartment of Molecular Embryology, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg D-79104, Germany.
Eleni RoussaDepartment of Molecular Embryology, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg D-79104, Germany.
Belal RahhalDepartment of Molecular Embryology, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg D-79104, Germany.
Aimee ZunigaDevelopmental Genetics, University of Basel Medical School, Basel CH-4058, Switzerland.
Kerstin KrieglsteinDepartment of Molecular Embryology, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg D-79104, Germany.
Joachim WittbrodtCentre for Organismal Studies, Heidelberg D-69120, Germany.
Stephan HeermannDepartment of Molecular Embryology, Institute of Anatomy and Cell Biology, Faculty of Medicine, University of Freiburg, Freiburg D-79104, Germany stephan.heermann@anat.uni-freiburg.de.ORCID 0000-0001-7374-8886
University of Freiburg · DEUniversidad de Oviedo · ESUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The optic fissure is a transient gap in the developing vertebrate eye, which must be closed as development proceeds. A persisting optic fissure, coloboma, is a major cause for blindness in children. Although many genes have been linked to coloboma, the process of optic fissure fusion is still little appreciated, especially on a molecular level. We identified a coloboma in mice with a targeted inactivation of transforming growth factor β2 (TGFβ2). Notably, here the optic fissure margins must have touched, however failed to fuse. Transcriptomic analyses indicated an effect on remodelling of the extracellular matrix (ECM) as an underlying mechanism. TGFβ signalling is well known for its effect on ECM remodelling, but it is at the same time often inhibited by bone morphogenetic protein (BMP) signalling. Notably, we also identified two BMP antagonists among the downregulated genes. For further functional analyses we made use of zebrafish, in which we found TGFβ ligands expressed in the developing eye, and the ligand binding receptor in the optic fissure margins where we also found active TGFβ signalling and, notably, also gremlin 2b (

Indexed as

AnimalsBone Morphogenetic ProteinsColobomaDisease Models, AnimalExtracellular MatrixFollistatinGene Expression ProfilingIntercellular Signaling Peptides and ProteinsMiceSignal TransductionTransforming Growth Factor beta2ZebrafishZebrafish ProteinsBone Morphogenetic ProteinsFollistatingrem2b protein, zebrafishIntercellular Signaling Peptides and ProteinsTgfb2 protein, mouseTransforming Growth Factor beta2Zebrafish ProteinsBMPcolobomaECMoptic fissure fusionTGFβ

Identifiers

PMID29593116
PMCPMC5881030
OpenAlexW2794885750

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.