Evidence map›Paper›PMID 25511461›Full record

ArticleMechanisms of development2015

Disrupting Foxh1-Groucho interaction reveals robustness of nodal-based embryonic patterning.

Angela M Halstead, Christopher V E Wright

Abstract read
In one paragraph

Article in Mechanisms of development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. FoxH1 Represses the Promoter Activity ofInternational journal of molecular sciences · 2023
    Article
  2. Article
  3. Review
  4. Article
  5. 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

2 authors.

Angela M HalsteadDepartment of Cell and Developmental Biology, Program in Developmental Biology, Center for Stem Cell Biology, Vanderbilt University Medical School, 2213 Garland Ave., Nashville, TN 37232, United States.
Christopher V E WrightDepartment of Cell and Developmental Biology, Program in Developmental Biology, Center for Stem Cell Biology, Vanderbilt University Medical School, 2213 Garland Ave., Nashville, TN 37232, United States. Electronic address: chris.wright@vanderbilt.edu.

Funding

Tumor Immunology and Microenvironment Research ProgramP30CA068485 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MATTHEW J TYSKA · 1995 to 2026
$172.8M
Vanderbilt Diabetes Research CenterP30DK020593 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI OWEN P MCGUINNESS · 2012 to 2026
$29.3M
TRANSGENIC MOUSE/ ES CELL SHARES RESOURCESP60DK020593 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1986 to 2011
$28.1M
BIOLOGICAL ROLES OF NODAL RELATED GENES IN EMBRYOGENESISR01GM056238 · NIGMS · VANDERBILT UNIVERSITY · PI WRIGHT, CHRISTOPHER V · 1997 to 2010
$2.8M
NCI NIH HHS CA68485NCI NIH HHS P30 CA068485NIDDK NIH HHS DK20593NIDDK NIH HHS P30 DK020593NIDDK NIH HHS P60 DK020593NIGMS NIH HHS R01 GM056238NIGMS NIH HHS R01GM56238
6 · The paper itself

Abstract

The winged-helix transcription factor Foxh1 is an essential regulator of Nodal signaling during the key developmental processes of gastrulation, anterior-posterior (A-P) patterning, and the derivation of left-right (L-R) asymmetry. Current models have Foxh1 bound to phospho-Smad2/3 (pSmad2/3) as a central transcriptional activator for genes targeted by Nodal signaling including Nodal itself, the feedback inhibitor Lefty2, and the positive transcriptional effector Pitx2. However, the conserved Engrailed homology-1 (EH1) motif present in Foxh1 suggests that modulated interaction with Groucho (Grg) co-repressors would allow Foxh1 to function as a transcriptional switch, toggling between transcriptional on and off states via pSmad2-Grg protein-switching, to ensure the properly timed initiation and suppression, and/or amplitude, of expression of Nodal and its target genes. We minimally mutated the Foxh1 EH1 motif, creating a novel Foxh1(mEH1) allele to test directly the contribution of Foxh1-Grg-mediated repression on the transient, dynamic pattern of Nodal signaling in mice. All aspects of Nodal and its target gene expression in Foxh1(mEH1/mEH1) embryos were equivalent to wild type. A-P patterning and organ situs in homozygous embryos and adult mice were also unaffected. The finding that Foxh1-Grg-mediated repression is not essential for Nodal expression during mouse embryogenesis suggests that other regulators compensate for the loss of repressive regulatory input that is mediated by Grg interactions. We suggest that the pervasive inductive properties of Nodal signaling exist within the context of a strongly buffered regulatory system that contributes to resilience and accuracy of its dynamic expression pattern.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBody PatterningCo-Repressor ProteinsEmbryonic DevelopmentForkhead Transcription FactorsGastrulationMiceNodal ProteinTranscription FactorsCo-Repressor ProteinsForkhead Transcription FactorsFoxh1 protein, mouseNodal ProteinTle5 protein, mouseTranscription FactorsEmbryonic patterningFoxh1GrouchoNodalTranscriptional regulation

Identifiers

PMID25511461
PMCPMC4747026

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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.