Evidence map›Paper›PMID 23283339›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Rax is a selector gene for mediobasal hypothalamic cell types.

Fuqu Lu, Deepon Kar, Nicole Gruenig, Zi Wei Zhang, Nicole Cousins, Helen M Rodgers, Eric C Swindell, Milan Jamrich, Carol Schuurmans, Peter H Mathers and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 79 citations in OpenAlex.

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  17. The rax homeobox gene is mutated in the eyeless axolotl, Ambystoma mexicanum.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
  18. Article
  19. Review
  20. A Highly ConservedFrontiers in cell and developmental biology · 2021
    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 5 institutions in 2 countries.

Fuqu LuDepartment of Medical Genetics, Alberta Children's Hospital Research Institute, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Deepon Kar
Nicole Gruenig
Zi Wei Zhang
Nicole Cousins
Helen M Rodgers
Eric C Swindell
Milan Jamrich
Carol Schuurmans
Peter H Mathers
Deborah M Kurrasch
Alberta Children's Hospital · CAUniversity of Calgary · CAWest Virginia University · USBaylor Genetics · USTexas Medical Center · US

Funding

Molecular control of retinal stem cell developmentR01EY012152 · NEI · WEST VIRGINIA UNIVERSITY · PI MATHERS, PETER H · 2005 to 2007
$968k
MOLECULAR CONTROL OF RETINAL STEM CELL DEVELOPMENTR29EY012152 · NEI · WEST VIRGINIA UNIVERSITY · PI MATHERS, PETER H · 1998 to 2002
$316k
CIHR MOP-275053CIHR MOP-44094NEI NIH HHS EY012152NEI NIH HHS R01 EY012152NEI NIH HHS R29 EY012152
6 · The paper itself

Abstract

The brain plays a central role in controlling energy, glucose, and lipid homeostasis, with specialized neurons within nuclei of the mediobasal hypothalamus, namely the arcuate (ARC) and ventromedial (VMH), tasked with proper signal integration. Exactly how the exquisite cytoarchitecture and underlying circuitry becomes established within these nuclei remains largely unknown, in part because hypothalamic developmental programs are just beginning to be elucidated. Here, we demonstrate that the Retina and anterior neural fold homeobox (Rax) gene plays a key role in establishing ARC and VMH nuclei in mice. First, we show that Rax is expressed in ARC and VMH progenitors throughout development, consistent with genetic fate mapping studies demonstrating that Rax+ lineages give rise to VMH neurons. Second, the conditional ablation of Rax in a subset of VMH progenitors using a Shh::Cre driver leads to a fate switch from a VMH neuronal phenotype to a hypothalamic but non-VMH identity, suggesting that Rax is a selector gene for VMH cellular fates. Finally, the broader elimination of Rax throughout ARC/VMH progenitors using Six3::Cre leads to a severe loss of both VMH and ARC cellular phenotypes, demonstrating a role for Rax in both VMH and ARC fate specification. Combined, our study illustrates that Rax is required in ARC/VMH progenitors to specify neuronal phenotypes within this hypothalamic brain region. Rax thus provides a molecular entry point for further study of the ontology and establishment of hypothalamic feeding circuits.

Indexed as

AnimalsCell LineageEye ProteinsGene Expression Regulation, DevelopmentalHomeodomain ProteinsHypothalamus, MiddleMiceMice, TransgenicNeuronsSignal TransductionTranscription FactorsEye ProteinsHomeodomain ProteinsRax protein, mouseTranscription Factors

Identifiers

PMID23283339
PMCPMC3582370
OpenAlexW2068568571

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.