Evidence map›Paper›PMID 25915473›Full record

ArticleNature neuroscience2015

Tet3 regulates synaptic transmission and homeostatic plasticity via DNA oxidation and repair.

Huimei Yu, Yijing Su, Jaehoon Shin, Chun Zhong, Junjie U Guo, Yi-Lan Weng, Fuying Gao, Daniel H Geschwind, Giovanni Coppola, Guo-li Ming and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 202 citations in OpenAlex.

  1. Review
  2. A distinct subclade of AlkB family demethylases in ciliates safeguards the positional fidelity of eukaryotic NProceedings of the National Academy of Sciences of the United States of America · 2026
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  11. Article
  12. DNA Methylation in Long-Term Memory.Physiology (Bethesda, Md.) · 2025
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
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65 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Huimei Yu1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yijing Su1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Jaehoon Shin1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Graduate Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Chun Zhong1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Junjie U Guo1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.ORCID 0000000188710055
Yi-Lan Weng1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Fuying Gao1] Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [2] Program in Neurogenetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [3] Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [4] Department of Psychiatry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
Daniel H Geschwind1] Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [2] Program in Neurogenetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [3] Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [4] Department of Psychiatry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.
Giovanni Coppola1] Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [2] Program in Neurogenetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [3] Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA. [4] Department of Psychiatry, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA.ORCID 0000000321051061
Guo-li Ming1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [3] Graduate Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [4] The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [5] Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Hongjun Song1] Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [2] Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [3] Graduate Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. [4] The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USUniversity of California, Los Angeles · US

Funding

Integrative Center for Neurogenetics and Neurogenomics - OverallP30NS062691 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COPPOLA, GIOVANNI · 2009 to 2018
$7.4M
Development of new neurons in the adult brainR01NS047344 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SONG, HONGJUN · 2003 to 2011
$3.4M
Calcium signaling in neuronal navigationR01NS048271 · NINDS · JOHNS HOPKINS UNIVERSITY · PI MING, GUO-LI · 2004 to 2014
$3.2M
Local circuitry mechanisms regulating adult hippocampal neurogenesisR37NS047344 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SONG, HONGJUN · 2013 to 2019
$2.9M
Circuitry mechanisms underlying normal and aberrant adult hippocampal neurogenesisR01MH105128 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI MING, GUO-LI · 2014 to 2018
$2.0M
Regulation of adult neurogenesis during agingR01AG024984 · NIA · JOHNS HOPKINS UNIVERSITY · PI SONG, HONGJUN · 2004 to 2008
$1.6M
Neural Development of Human Induced Pluripotent Stem Cells from Schizophrenia PatR33MH087874 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SONG, HONGJUN · 2011 to 2012
$805k
Impact of Bisphenol A on neural stem cells and development in the adult brainR21ES021957 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI SONG, HONGJUN · 2012 to 2013
$441k
Circuitry mechanisms regulating adult hippocampal neurogenesisR56NS047344 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SONG, HONGJUN · 2012 to 2012
$405k
NIA NIH HHS R01 AG024984NIEHS NIH HHS R21 ES021957NIMH NIH HHS MH105128NIMH NIH HHS R01 MH105128NIMH NIH HHS R33 MH087874NINDS NIH HHS NS047344NINDS NIH HHS NS048271NINDS NIH HHS NS062691NINDS NIH HHS P30 NS062691NINDS NIH HHS R01 NS047344NINDS NIH HHS R01 NS048271NINDS NIH HHS R37 NS047344NINDS NIH HHS R56 NS047344
6 · The paper itself

Abstract

Contrary to the long-held belief that DNA methylation of terminally differentiated cells is permanent and essentially immutable, post-mitotic neurons exhibit extensive DNA demethylation. The cellular function of active DNA demethylation in neurons, however, remains largely unknown. Tet family proteins oxidize 5-methylcytosine to initiate active DNA demethylation through the base-excision repair (BER) pathway. We found that synaptic activity bi-directionally regulates neuronal Tet3 expression. Functionally, knockdown of Tet or inhibition of BER in hippocampal neurons elevated excitatory glutamatergic synaptic transmission, whereas overexpressing Tet3 or Tet1 catalytic domain decreased it. Furthermore, dysregulation of Tet3 signaling prevented homeostatic synaptic plasticity. Mechanistically, Tet3 dictated neuronal surface GluR1 levels. RNA-seq analyses further revealed a pivotal role of Tet3 in regulating gene expression in response to global synaptic activity changes. Thus, Tet3 serves as a synaptic activity sensor to epigenetically regulate fundamental properties and meta-plasticity of neurons via active DNA demethylation.

Indexed as

AnimalsDioxygenasesDNADNA-Binding ProteinsDNA MethylationDNA RepairGene Knockdown TechniquesHomeostasisIn Vitro TechniquesMiceMice, Inbred C57BLNeuronal PlasticityOxidation-ReductionProto-Oncogene ProteinsReceptors, AMPASignal TransductionDioxygenasesDNADNA-Binding ProteinsProto-Oncogene ProteinsReceptors, AMPATet3 protein, mouse

Identifiers

PMID25915473
PMCPMC4446239
OpenAlexW2008060564

What OpenQuestion holds

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Registered trials

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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.