Evidence map›Paper›PMID 9250683›Full record

ArticleThe EMBO journal1997

Deletion of a HoxD enhancer induces transcriptional heterochrony leading to transposition of the sacrum.

J Zákány, M Gérard, B Favier, D Duboule

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 113 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Hox genes in the adult skeleton: Novel functions beyond embryonic development.Developmental dynamics : an official publication of the American Association of Anatomists · 2017
    Review
  11. Article
  12. Article
  13. Hoxa5: A Key Player in Development and Disease.Journal of developmental biology · 2016
    Review
  14. Independent regulation of vertebral number and vertebral identity by microRNA-196 paralogs.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  15. MOZ and BMI1 play opposing roles during Hox gene activation in ES cells and in body segment identity specification in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  16. Article
  17. The chromatin insulator CTCF and the emergence of metazoan diversity.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. Article
  19. Transcriptional neoteny in the human brain.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  20. 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

4 authors at 1 institution in 1 country.

J ZákányDepartment of Zoology and Animal Biology, University of Geneva, Sciences III, Switzerland.
M Gérard
B Favier
D Duboule
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A phylogenetically conserved transcriptional enhancer necessary for the activation of Hoxd-11 was deleted from the HoxD complex of mice by targeted mutagenesis. While genetic and expression analyses demonstrated the role of this regulatory element in the activation of Hoxd-11 during early somitogenesis, the function of this gene in developing limbs and the urogenital system was not affected, suggesting that Hox transcriptional controls are different in different axial structures. In the trunk of mutant embryos, transcriptional activation of Hoxd-11 and Hoxd-10 was severely delayed, but subsequently resumed with appropriate spatial distributions. The resulting caudal transposition of the sacrum indicates that proper vertebral specification requires a precise temporal control of Hox gene expression, in addition to spatial regulation. A slight time delay in expression (transcriptional heterochrony) cannot be compensated for at a later developmental stage, eventually leading to morphological alterations.

Indexed as

Genes, HomeoboxTranscription, GeneticAnimalsCell LineEnhancer Elements, GeneticForelimbGene Expression Regulation, DevelopmentalHomeodomain ProteinsIn Situ HybridizationMiceMice, TransgenicMutagenesis, InsertionalSacrumSequence DeletionTranscription FactorsHomeodomain ProteinsHoxd11 protein, mouseTranscription Factors

Identifiers

PMID9250683
PMCPMC1170065
OpenAlexW2071789449

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.