Evidence map›Paper›PMID 24671995›Full record

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

Coordinated regulation of dendrite arborization by epigenetic factors CDYL and EZH2.

Cai Qi, Shumeng Liu, Rui Qin, Yu Zhang, Guoqiang Wang, Yongfeng Shang, Yun Wang, Jing Liang

Erratum issuedOpen 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. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Emerging roles for E3 ubiquitin ligases in neural development and disease.Frontiers in cell and developmental biology · 2025
    Review
  5. Article
  6. Review
  7. The Roles of H3K9me3 Writers, Readers, and Erasers in Cancer Immunotherapy.International journal of molecular sciences · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. CDYL reinforces male gonadal sex determination through epigenetically repressingProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Cai QiNeuroscience Research Institute, Department of Neurobiology, School of Basic Medical Sciences, Key Laboratory for Neuroscience, Ministry of Education/National Health and Family Planning Commission and Key Laboratory of Carcinogenesis and Translational Research (Ministry of Education), Department of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100191, China, Tianjin Key Laboratory of Medical Epigenetics, Tianjin Medical University, Tianjin 300070, China, and PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China.
Shumeng Liu
Rui Qin
Yu Zhang
Guoqiang Wang
Yongfeng Shang
Yun Wang
Jing Liang
National Health and Family Planning Commission · CNPeking University · CNTianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dendritic arborization is one of the key determinants of precise circuits for information processing in neurons. Unraveling the molecular mechanisms underlying dendrite morphogenesis is critical to understanding the establishment of neuronal connections. Here, using gain- and loss-of-function approaches, we defined the chromodomain protein and transcription corepressor chromodomain Y-like (CDYL) protein as a negative regulator of dendrite morphogenesis in rat/mouse hippocampal neurons both in vitro and in vivo. Overexpressing CDYL decreased, whereas knocking it down increased, the dendritic complexity of the primary cultured rat neurons. High-throughput DNA microarray screening identified a number of CDYL downstream target genes, including the brain-derived neurotrophic factor (BDNF). Knock-down of CDYL in neuronal cells led to increased expression of BDNF, which is primarily responsible for CDYL's effects on dendrite patterns. Mechanistically, CDYL interacts with EZH2, the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), directly and recruits the H3K27 methyltransferase activity to the promoter region of the BDNF gene. In doing so, CDYL and EZH2 coordinately restrict dendrite morphogenesis in an interdependent manner. Finally, we found that neural activity increased dendritic complexity through degradation of CDYL protein to unleash its inhibition on BDNF. These results link, for the first time, the epigenetic regulators CDYL and EZH2 to dendrite morphogenesis and might shed new light on our understanding of the regulation of the neurodevelopment.

Indexed as

AnimalsCells, CulturedCo-Repressor ProteinsDendritesEmbryo, MammalianEnhancer of Zeste Homolog 2 ProteinFemaleGene Expression Regulation, DevelopmentalHippocampusHumansHydro-LyasesMaleMiceMice, Inbred ICRMice, TransgenicMutationCDYL protein, humanCo-Repressor ProteinsEnhancer of Zeste Homolog 2 ProteinEZH2 protein, humanHydro-LyasesPolycomb Repressive Complex 2ProteinsRNA, Small Interfering

Identifiers

PMID24671995
PMCPMC6608133
OpenAlexW2030615857

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.