Evidence map›Paper›PMID 39395911›Full record

ArticleNeuroscience bulletin2024

Loss of TET Activity in the Postnatal Mouse Brain Perturbs Synaptic Gene Expression and Impairs Cognitive Function.

Ji-Wei Liu, Ze-Qiang Zhang, Zhi-Chuan Zhu, Kui Li, Qiwu Xu, Jing Zhang, Xue-Wen Cheng, Han Li, Ying Sun, Ji-Jun Wang and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuroscience bulletin, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Special Issue Celebrating the 25Neuroscience bulletin · 2024
    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

13 authors.

Ji-Wei Liu *Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Ze-Qiang Zhang *University of Chinese Academy of Sciences, Beijing, 100049, China.
Zhi-Chuan ZhuInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 20031, China.
Kui LiInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 20031, China.
Qiwu XuInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 20031, China.
Jing ZhangInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 20031, China.
Xue-Wen ChengInstitute of Neuroscience, State Key Laboratory of Neuroscience, Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 20031, China.
Han LiShanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Ying SunShanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Ji-Jun WangShanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Lu-Lu HuFudan University Institutes of Biomedical Sciences, Shanghai Cancer Center, Shanghai Key Laboratory of Medical Epigenetics, International Co-laboratory of Medical Epigenetics and Metabolism (Ministry of Science and Technology), Shanghai Medical College of Fudan University, Shanghai, 200032, China.
Zhi-Qi XiongUniversity of Chinese Academy of Sciences, Beijing, 100049, China. xiongzhiqi@ion.ac.cn.
Yongchuan ZhuShanghai Key Laboratory of Psychotic Disorders, Shanghai Mental Health Center, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. yczhu@smhc.org.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC) by ten-eleven translocation (TET) family proteins leads to the accumulation of 5hmC in the central nervous system; however, the role of 5hmC in the postnatal brain and how its levels and target genes are regulated by TETs remain elusive. We have generated mice that lack all three Tet genes specifically in postnatal excitatory neurons. These mice exhibit significantly reduced 5hmC levels, altered dendritic spine morphology within brain regions crucial for cognition, and substantially impaired spatial and associative memories. Transcriptome profiling combined with epigenetic mapping reveals that a subset of genes, which display changes in both 5hmC/5mC levels and expression patterns, are involved in synapse-related functions. Our findings provide insight into the role of postnatally accumulated 5hmC in the mouse brain and underscore the impact of 5hmC modification on the expression of genes essential for synapse development and function.

Indexed as

5-MethylcytosineBrainSynapsesAnimalsCognitionDioxygenasesDNA-Binding ProteinsEpigenesis, GeneticGene ExpressionMiceMice, Inbred C57BLMice, KnockoutMixed Function OxygenasesProto-Oncogene Proteins5-hydroxymethylcytosine5-MethylcytosineDioxygenasesDNA-Binding ProteinsMixed Function OxygenasesProto-Oncogene ProteinsTET1 protein, mouseTet2 protein, mouseTet3 protein, mouse5hmCDNA demethylationEpigeneticsLearning and memorySynapseTET

Identifiers

PMID39395911
PMCPMC11607366

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.