Evidence map›Paper›PMID 19168674›Full record

ArticleDevelopment (Cambridge, England)2009

Sall genes regulate region-specific morphogenesis in the mouse limb by modulating Hox activities.

Yasuhiko Kawakami, Yukako Uchiyama, Concepcion Rodriguez Esteban, Toshiaki Inenaga, Naoko Koyano-Nakagawa, Hiroko Kawakami, Merce Marti, Marie Kmita, Paula Monaghan-Nichols, Ryuichi Nishinakamura and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Development (Cambridge, England), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

11 authors at 3 institutions in 2 countries.

Yasuhiko KawakamiGene Expression Laboratory, The Salk Institute for Biological Studies, La Jolla, CA 92037, USA.
Yukako Uchiyama
Concepcion Rodriguez Esteban
Toshiaki Inenaga
Naoko Koyano-Nakagawa
Hiroko Kawakami
Merce Marti
Marie Kmita
Paula Monaghan-Nichols
Ryuichi Nishinakamura
Juan Carlos Izpisua Belmonte
Salk Institute for Biological Studies · USMontreal Clinical Research Institute · CAUniversity of Pittsburgh · US

Funding

MOLECULAR GENETIC ANALYSIS OF FOREBRAIN DEVELOPMENTR01MH060774 · NIMH · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MONAGHAN-NICHOLS, A PAULA · 2000 to 2008
$2.3M
CIHR 82880-1CIHR 83362-1NIMH NIH HHS R01 MH060774
6 · The paper itself

Abstract

The genetic mechanisms that regulate the complex morphogenesis of generating cartilage elements in correct positions with precise shapes during organogenesis, fundamental issues in developmental biology, are still not well understood. By focusing on the developing mouse limb, we confirm the importance of transcription factors encoded by the Sall gene family in proper limb morphogenesis, and further show that they have overlapping activities in regulating regional morphogenesis in the autopod. Sall1/Sall3 double null mutants exhibit a loss of digit1 as well as a loss or fusion of digit2 and digit3, metacarpals and carpals in the autopod. We show that Sall activity affects different pathways, including the Shh signaling pathway, as well as the Hox network. Shh signaling in the mesenchyme is partially impaired in the Sall mutant limbs. Additionally, our data suggest an antagonism between Sall1-Sall3 and Hoxa13-Hoxd13. We demonstrate that expression of Epha3 and Epha4 is downregulated in the Sall1/Sall3 double null mutants, and, conversely, is upregulated in Hoxa13 and Hoxd13 mutants. Moreover, the expression of Sall1 and Sall3 is upregulated in Hoxa13 and Hoxd13 mutants. Furthermore, by using DNA-binding assays, we show that Sall and Hox compete for a target sequence in the Epha4 upstream region. In conjunction with the Shh pathway, the antagonistic interaction between Hoxa13-Hoxd13 and Sall1-Sall3 in the developing limb may contribute to the fine-tuning of local Hox activity that leads to proper morphogenesis of each cartilage element of the vertebrate autopod.

Indexed as

MorphogenesisAnimalsExtremitiesGene Expression Regulation, DevelopmentalHedgehog ProteinsHomeodomain ProteinsKruppel-Like Transcription FactorsMiceMutationNerve Tissue ProteinsOrgan SpecificityReceptor, EphA3Receptor, EphA4Signal TransductionT-Box Domain ProteinsTranscription FactorsEpha3 protein, mouseGli3 protein, mouseHedgehog Proteinshomeobox protein HOXA13Homeodomain ProteinsHoxd13 protein, mouseKruppel-Like Transcription FactorsNerve Tissue ProteinsReceptor, EphA3Receptor, EphA4Sall1 protein, mouseSall3 protein, mouseShh protein, mouseT-Box Domain ProteinsT-box transcription factor 5Transcription FactorsZinc Finger Protein Gli3

Identifiers

PMID19168674
PMCPMC3266482
OpenAlexW2045216907

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.