Evidence map›Paper›PMID 24008197›Full record

ArticleDevelopmental biology2013

Zebrafish Tbx16 regulates intermediate mesoderm cell fate by attenuating Fgf activity.

Rachel M Warga, Rachel L Mueller, Robert K Ho, Donald A Kane

Open access · greenAbstract read
In one paragraph

Article in Developmental biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Disrupted developmental signaling induces novel transcriptional states.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  10. Fgf-driven Tbx protein activities directly induceDevelopment (Cambridge, England) · 2020
    Article
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  13. tbx6l and tbx16 are redundantly required for posterior paraxial mesoderm formation during zebrafish embryogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
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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

4 authors at 2 institutions in 1 country.

Rachel M WargaDepartment of Biological Sciences, Western Michigan University, Kalamazoo, MI 49008, USA; Department of Organismal Biology and Anatomy, University of Chicago, 1027 East, 57th Street, Chicago, IL 60637, USA. Electronic address: rachel.warga@wmich.edu.
Rachel L Mueller
Robert K Ho
Donald A Kane
University of Chicago · USWestern Michigan University · US

Funding

Segmentation Defects in Vertebrate Paraxial MesodermR01GM067714 · NIGMS · UNIVERSITY OF CHICAGO · PI HO, ROBERT K · 2002 to 2011
$2.5M
An Animal Model for Human Heart-Hand SyndromesR01HD072598 · NICHD · UNIVERSITY OF CHICAGO · PI HO, ROBERT K · 2013 to 2017
$1.6M
Specification of blood lineages in a vertebrate embryoR01DK068286 · NIDDK · UNIVERSITY OF CHICAGO · PI HO, ROBERT K · 2004 to 2008
$1.3M
NICHD NIH HHS R01 HD072598NIDDK NIH HHS R01 DK068286NIDDK NIH HHS R01-DK68286NIGMS NIH HHS R01 GM067714NIGMS NIH HHS R01-GM067714
6 · The paper itself

Abstract

Progenitors of the zebrafish pronephros, red blood and trunk endothelium all originate from the ventral mesoderm and often share lineage with one another, suggesting that their initial patterning is linked. Previous studies have shown that spadetail (spt) mutant embryos, defective in tbx16 gene function, fail to produce red blood cells, but retain the normal number of endothelial and pronephric cells. We report here that spt mutants are deficient in all the types of early blood, have fewer endothelial cells as well as far more pronephric cells compared to wildtype. In vivo cell tracing experiments reveal that blood and endothelium originate in spt mutants almost exclusive from the dorsal mesoderm whereas, pronephros and tail originate from both dorsal and ventral mesoderm. Together these findings suggest possible defects in posterior patterning. In accord with this, gene expression analysis shows that mesodermal derivatives within the trunk and tail of spt mutants have acquired more posterior identity. Secreted signaling molecules belonging to the Fgf, Wnt and Bmp families have been implicated as patterning factors of the posterior mesoderm. Further investigation demonstrates that Fgf and Wnt signaling are elevated throughout the nonaxial region of the spt gastrula. By manipulating Fgf signaling we show that Fgfs both promote pronephric fate and repress blood and endothelial fate. We conclude that Tbx16 plays an important role in regulating the balance of intermediate mesoderm fates by attenuating Fgf activity.

Indexed as

AnimalsCell DifferentiationDNA PrimersFibroblast Growth FactorsGene Expression ProfilingIn Situ HybridizationMesodermPronephrosT-Box Domain ProteinsWnt Signaling PathwayZebrafishZebrafish ProteinsDNA PrimersFibroblast Growth FactorsT-Box Domain Proteinstbx16 protein, zebrafishZebrafish ProteinsBloodEndotheliumFgf8Intermediate mesodermPronephrosTbx16

Identifiers

PMID24008197
PMCPMC3919442
OpenAlexW1971004619

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.