Evidence map›Paper›PMID 30063881›Full record

ArticleDevelopmental biology2018

Canonical Wnt signaling regulates patterning, differentiation and nucleogenesis in mouse hypothalamus and prethalamus.

Elizabeth A Newman, Dan Wu, Makoto Mark Taketo, Jiangyang Zhang, Seth Blackshaw

Abstract read
In one paragraph

Article in Developmental biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. CTNNB1 syndrome mouse models.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
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  20. The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    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

5 authors at 3 institutions in 2 countries.

Elizabeth A NewmanSolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Dan WuDepartment of Radiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Makoto Mark TaketoDivision of Experimental Therapeutics, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Jiangyang ZhangDepartment of Radiology, NYU Langone School of Medicine, New York, NY, USA.
Seth BlackshawSolomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Ophthalmology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Center for Human Systems Biology, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, USA. Electronic address: sblack@jhmi.edu.
Johns Hopkins University · USKyoto University · JPNew York University · US

Funding

TR&D 4: Revealing Microstructure: Biophysical modeling and validation for discovery and clinical careP41EB017183 · NIBIB · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Hersh Chandarana · 2014 to 2026
$19.3M
The Function and Regulation of Tanycyte-Derived Hypothalamic NeurogenesisR01DK108230 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI BLACKSHAW, SETH · 2016 to 2019
$1.5M
NIBIB NIH HHS P41 EB017183NIDDK NIH HHS R01 DK108230
6 · The paper itself

Abstract

The hypothalamus is a small, but anatomically and functionally complex region of the brain whose development is poorly understood. In this study, we have explored its development by studying the canonical Wnt signaling pathway, generating gain and loss of function mutations of beta-catenin (Ctnnb1) in both hypothalamic and prethalamic neuroepithelium. Deletion of Ctnnb1 resulted in an anteriorized and hypoplastic hypothalamus. Posterior structures were lost or reduced, and anterior structures were expanded. In contrast, overexpression of a constitutively active mutant form of Ctnnb1 resulted in severe hyperplasia of prethalamus and hypothalamus, and expanded expression of a subset of posterior and premamillary hypothalamic markers. Moderate defects in differentiation of Arx-positive GABAergic neural precursors were observed in both prethalamus and hypothalamus of Ctnnb1 loss of function mutants, while in gain of function mutants, their differentiation was completely suppressed, although markers of prethalamic progenitors were preserved. Multiple other region-specific markers, including several specific posterior hypothalamic structures, were also suppressed in Ctnnb1 gain of function mutations. Severe, region-specific defects in hypothalamic nucleogenesis were also observed in both gain and loss of function mutations of Ctnnb1. Finally, both gain and loss of function of Ctnnb1 also produced severe, non-cell autonomous disruptions of pituitary development. These findings demonstrate a central and multifaceted role for canonical Wnt signaling in regulating growth, patterning, differentiation and nucleogenesis in multiple diencephalic regions.

Indexed as

Animalsbeta CateninBody PatterningCell DifferentiationFemaleHypothalamusMaleMiceMice, TransgenicPregnancyWnt Signaling Pathwaybeta CateninCTNNB1 protein, mouse

Identifiers

PMID30063881
PMCPMC6143395
OpenAlexW2953048462

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.