Evidence map›Paper›PMID 24553927›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Dual effect of CTCF loss on neuroprogenitor differentiation and survival.

L Ashley Watson, Xu Wang, Adrienne Elbert, Kristin D Kernohan, Niels Galjart, Nathalie G Bérubé

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. An updated catalog ofFrontiers in molecular neuroscience · 2023
    Pooled it
  2. Article
  3. Article
  4. Article
  5. CTCF regulates global chromatin accessibility and transcription during rod photoreceptor development.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Expanding GABAergic Neuronal Diversity in iPSC-Derived Disease Models.bioRxiv : the preprint server for biology · 2024
    Article
  7. Genetic association ofTranslational pediatrics · 2024
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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

6 authors at 3 institutions in 2 countries.

L Ashley WatsonDepartments of Paediatrics and Biochemistry, The University of Western Ontario and Children's Health Research Institute, London, Ontario N6C 2V5, Canada and Medical Genetics Centre Department of Cell Biology and Genetics, Erasmus University, 3000 CA, Rotterdam, The Netherlands.
Xu Wang
Adrienne Elbert
Kristin D Kernohan
Niels Galjart
Nathalie G Bérubé
Children’s Health Research Institute · CAWestern University · CAErasmus MC · NL

Funding

Canadian Institutes of Health Research MOP93697
6 · The paper itself

Abstract

An increasing number of proteins involved in genome organization have been implicated in neurodevelopmental disorders, highlighting the importance of chromatin architecture in the developing CNS. The CCCTC-binding factor (CTCF) is a zinc finger DNA binding protein involved in higher-order chromatin organization, and mutations in the human CTCF gene cause an intellectual disability syndrome associated with microcephaly. However, information on CTCF function in vivo in the developing brain is lacking. To address this gap, we conditionally inactivated the Ctcf gene at early stages of mouse brain development. Cre-mediated Ctcf deletion in the telencephalon and anterior retina at embryonic day 8.5 triggered upregulation of the p53 effector PUMA (p53 upregulated modulator of apoptosis), resulting in massive apoptosis and profound ablation of telencephalic structures. Inactivation of Ctcf several days later at E11 also resulted in PUMA upregulation and increased apoptotic cell death, and the Ctcf-null forebrain was hypocellular and disorganized at birth. Although deletion of both Ctcf and Puma in the embryonic brain efficiently rescued Ctcf-null progenitor cell apoptosis, it failed to improve neonatal hypocellularity due to decreased proliferative capacity of rescued apical and outer radial glia progenitor cells. This was exacerbated by an independent effect of CTCF loss that resulted in depletion of the progenitor pool due to premature neurogenesis earlier in development. Our findings demonstrate that CTCF activities are required for two distinct events in early cortex formation: first, to correctly regulate the balance between neuroprogenitor cell proliferation and differentiation, and second, for the survival of neuroprogenitor cells, providing new clues regarding the contributions of CTCF in microcephaly/intellectual disability syndrome pathologies.

Indexed as

AnimalsAntimetabolitesApoptosisApoptosis Regulatory ProteinsBrainBromodeoxyuridineCCCTC-Binding FactorCell DeathCell DifferentiationCell SurvivalChromatin ImmunoprecipitationExonsFemaleFluorescent Antibody TechniqueGenes, p53Image Processing, Computer-AssistedAntimetabolitesApoptosis Regulatory ProteinsBromodeoxyuridineCCCTC-Binding FactorCTCF protein, humanCtcf protein, mouseNestinPUMA protein, mouseRepressor ProteinsTumor Suppressor ProteinsapoptosisCTCFdifferentiationmouse modelneurogenesisPuma

Identifiers

PMID24553927
PMCPMC6608523
OpenAlexW2036066182

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.