Evidence map›Paper›PMID 32286661›Full record

ArticleNucleic acids research2020

Nono deficiency compromises TET1 chromatin association and impedes neuronal differentiation of mouse embryonic stem cells.

Wenjing Li, Violetta Karwacki-Neisius, Chun Ma, Li Tan, Yang Shi, Feizhen Wu, Yujiang Geno Shi

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

Article in Nucleic acids research, 2020. 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
1.3field-weighted citation impact, top 20% 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, 31 citations in OpenAlex.

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  12. RNA binding proteins in cardiovascular development and disease.Current topics in developmental biology · 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

7 authors at 3 institutions in 2 countries.

Wenjing LiLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China, and Key Laboratory of Birth Defects, Children's Hospital of Fudan University, Shanghai, 201102, China.
Violetta Karwacki-NeisiusDivision of Newborn Medicine and Program in Epigenetics, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA and Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.
Chun MaLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China, and Key Laboratory of Birth Defects, Children's Hospital of Fudan University, Shanghai, 201102, China.
Li TanLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China, and Key Laboratory of Birth Defects, Children's Hospital of Fudan University, Shanghai, 201102, China.
Yang ShiDivision of Newborn Medicine and Program in Epigenetics, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA and Department of Cell Biology, Harvard Medical School, 240 Longwood Avenue, Boston, MA 02115, USA.
Feizhen WuLaboratory of Epigenetics, Institutes of Biomedical Sciences, Fudan University, Shanghai, 200032, China, and Key Laboratory of Birth Defects, Children's Hospital of Fudan University, Shanghai, 201102, China.
Yujiang Geno ShiEndocrinology Division, Brigham and Women's Hospital, Harvard Medical School, 221 Longwood Avenue, Boston, MA 02115, USA.
Brigham and Women's Hospital · USChildren's Hospital of Fudan University · CNBoston Children's Hospital · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NONO is a DNA/RNA-binding protein, which plays a critical regulatory role during cell stage transitions of mouse embryonic stem cells (mESCs). However, its function in neuronal lineage commitment and the molecular mechanisms of its action in such processes are largely unknown. Here we report that NONO plays a key role during neuronal differentiation of mESCs. Nono deletion impedes neuronal lineage commitment largely due to a failure of up-regulation of specific genes critical for neuronal differentiation. Many of the NONO regulated genes are also DNA demethylase TET1 targeted genes. Importantly, re-introducing wild type NONO to the Nono KO cells, not only restores the normal expression of the majority of NONO/TET1 coregulated genes but also rescues the defective neuronal differentiation of Nono-deficient mESCs. Mechanistically, our data shows that NONO directly interacts with TET1 via its DNA binding domain and recruits TET1 to genomic loci to regulate 5-hydroxymethylcytosine levels. Nono deletion leads to a significant dissociation of TET1 from chromatin and dysregulation of DNA hydroxymethylation of neuronal genes. Taken together, our findings reveal a key role and an epigenetic mechanism of action of NONO in regulation of TET1-targeted neuronal genes, offering new functional and mechanistic understanding of NONO in stem cell functions, lineage commitment and specification.

Indexed as

5-MethylcytosineAnimalsCells, CulturedChromatinDNA-Binding ProteinsGene Expression RegulationGene Knockout TechniquesMiceMouse Embryonic Stem CellsNeurogenesisProto-Oncogene ProteinsRNA-Binding ProteinsRNA-SeqTranscription, Genetic5-hydroxymethylcytosine5-MethylcytosineChromatinDNA-Binding ProteinsNono protein, mouseProto-Oncogene ProteinsRNA-Binding ProteinsTET1 protein, mouse

Identifiers

PMID32286661
PMCPMC7229820
OpenAlexW3015554297

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.