Evidence map›Paper›PMID 18068699›Full record

ArticleDevelopmental biology2008

colgate/hdac1 Repression of foxd3 expression is required to permit mitfa-dependent melanogenesis.

Myron S Ignatius, Holly E Moose, Heithem M El-Hodiri, Paul D Henion

Open access · greenAbstract readComparative Study
In one paragraph

Article in Developmental biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
2.3field-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

42 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Review
  3. Exposure to valproic acid (VPA) reproducesmicroPublication biology · 2023
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Epigenetic Mechanisms in Hirschsprung Disease.International journal of molecular sciences · 2019
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. The melanocyte lineage in development and disease.Development (Cambridge, England) · 2015
    Review
  19. Review
  20. Review
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 1 institution in 1 country.

Myron S IgnatiusCenter for Molecular Neurobiology, Molecular, Cellular and Developmental Biology Program, Department of Neuroscience, The Ohio State University, 105 Rightmire Hall, 1060 Carmack Rd., Columbus, OH 43210, USA.
Holly E Moose
Heithem M El-Hodiri
Paul D Henion
The Ohio State University · US

Funding

Ohio State Neuroscience Centr CoreP30NS045758 · NINDS · OHIO STATE UNIVERSITY · PI MCTIGUE, DANA M · 2004 to 2015
$7.7M
The Role of Rx in Retinal Progenitor Cell DevelopmentR01EY015480 · NEI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI EL-HODIRI, HEITHEM M · 2004 to 2015
$3.7M
Development of Distinct Neural Crest and Hematopoietic SubpopulationsR01GM076505 · NIGMS · OHIO STATE UNIVERSITY · PI HENION, PAUL D · 2006 to 2009
$1.1M
NEI NIH HHS EY015480NEI NIH HHS R01 EY015480NIGMS NIH HHS R01 GM076505NINDS NIH HHS P30 NS045758NINDS NIH HHS P30-NS045758
6 · The paper itself

Abstract

Neural crest-derived pigment cell development has been used extensively to study cell fate specification, migration, proliferation, survival and differentiation. Many of the genes and regulatory mechanisms required for pigment cell development are conserved across vertebrates. The zebrafish mutant colgate (col)/histone deacetylase1 (hdac1) has reduced numbers, delayed differentiation and decreased migration of neural crest-derived melanophores and their precursors. In hdac1(col) mutants normal numbers of premigratory neural crest cells are induced. Later, while there is only a slight reduction in the number of neural crest cells in hdac1(col) mutants, there is a severe reduction in the number of mitfa-positive melanoblasts suggesting that hdac1 is required for melanoblast specification. Concomitantly, there is a significant increase in and prolonged expression of foxd3 in neural crest cells in hdac1(col) mutants. We found that partially reducing Foxd3 expression in hdac1(col) mutants rescues mitfa expression and the melanophore defects in hdac1(col) mutants. Furthermore, we demonstrate the ability of Foxd3 to physically interact at the mitfa promoter. Because mitfa is required for melanoblast specification and development, our results suggest that hdac1 is normally required to suppress neural crest foxd3 expression thus de-repressing mitfa resulting in melanogenesis by a subset of neural crest-derived cells.

Indexed as

Gene Expression Regulation, DevelopmentalAnimalsBase SequenceBinding SitesCell MovementElectrophoretic Mobility Shift AssayEmbryo, NonmammalianForkhead Transcription FactorsHistone Deacetylase 1Histone DeacetylasesIn Situ HybridizationMelanophoresMicroinjectionsMicrophthalmia-Associated Transcription FactorModels, BiologicalMolecular Sequence DataForkhead Transcription Factorsfoxd3 protein, zebrafishHDAC1 protein, zebrafishHistone Deacetylase 1Histone DeacetylasesMicrophthalmia-Associated Transcription Factormitfa protein, zebrafishOligonucleotides, AntisenseZebrafish Proteins

Identifiers

PMID18068699
PMCPMC2700343
OpenAlexW2092133045

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.