Evidence map›Paper›PMID 33086056›Full record

ArticleCell reports2020

CMTR1-Catalyzed 2'-O-Ribose Methylation Controls Neuronal Development by Regulating Camk2α Expression Independent of RIG-I Signaling.

Yen-Lurk Lee, Fan-Che Kung, Chia-Hsuan Lin, Yi-Shuian Huang

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. CMTr mediated 2'-RNA (New York, N.Y.) · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. CPEB3-dowregulated Nr3c1 mRNA translation confers resilience to developing posttraumatic stress disorder-like behavior in fear-conditioned mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  16. Review
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

4 authors at 2 institutions in 1 country.

Yen-Lurk LeeInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Taiwan International Graduate Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11529, Taiwan.
Fan-Che KungInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan.
Chia-Hsuan LinInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Yang-Ming University and Academia Sinica, Taipei 11529, Taiwan.
Yi-Shuian HuangInstitute of Biomedical Sciences, Academia Sinica, Taipei 11529, Taiwan; Taiwan International Graduate Program in Molecular Medicine, National Yang-Ming University and Academia Sinica, Taipei 11529, Taiwan; Taiwan International Graduate Program in Interdisciplinary Neuroscience, National Yang-Ming University and Academia Sinica, Taipei 11529, Taiwan. Electronic address: yishuian@ibms.sinica.edu.tw.
National Yang Ming Chiao Tung University · TWInstitute of Biomedical Sciences, Academia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eukaryotic mRNAs are 5' end capped with a 7-methylguanosine, which is important for processing and translation of mRNAs. Cap methyltransferase 1 (CMTR1) catalyzes 2'-O-ribose methylation of the first transcribed nucleotide (N1 2'-O-Me) to mask mRNAs from innate immune surveillance by retinoic-acid-inducible gene-I (RIG-I). Nevertheless, whether this modification regulates gene expression for neuronal functions remains unexplored. Here, we find that knockdown of CMTR1 impairs dendrite development independent of secretory cytokines and RIG-I signaling. Using transcriptomic analyses, we identify altered gene expression related to dendrite morphogenesis instead of RIG-I-activated interferon signaling, such as decreased calcium/calmodulin-dependent protein kinase 2α (Camk2α). In line with these molecular changes, dendritic complexity in CMTR1-insufficient neurons is rescued by ectopic expression of CaMK2α but not by inactivation of RIG-I signaling. We further generate brain-specific CMTR1-knockout mice to validate these findings in vivo. Our study reveals the indispensable role of CMTR1-catalyzed N1 2'-O-Me in gene regulation for brain development.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2DEAD Box Protein 58FemaleGene ExpressionGene Expression RegulationGuanosineMaleMethylationMethyltransferasesMiceMice, Inbred C57BLMice, KnockoutNeuronsRiboseRNA Caps7-methylguanosineCalcium-Calmodulin-Dependent Protein Kinase Type 2Camk2a protein, mouseDdx58 protein, mouseDEAD Box Protein 58GuanosineMethyltransferasesRiboseRNA CapsRNA, Messenger2′-O-ribose methylationCaMK2cap1 modificationCMTRdendrite developmentinnate immunityRIG-I

Identifiers

PMID33086056
PMCPMC7574844
OpenAlexW3093865703

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.