Evidence map›Paper›PMID 37769127›Full record

ArticleeLife2023

Coevolution of the CDCA7-HELLS ICF-related nucleosome remodeling complex and DNA methyltransferases.

Hironori Funabiki, Isabel E Wassing, Qingyuan Jia, Ji-Dung Luo, Thomas Carroll

Open access · goldAbstract read
In one paragraph

Article in eLife, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Oncology research · 2026
    Article
  5. CDCA7 facilitates MET1-mediated CG DNA methylation maintenance in centromeric heterochromatin via linker histone H1.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Article
  7. Sustainable integrative cell biology: CENP-C is guilty by association.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Hironori FunabikiLaboratory of Chromosome and Cell Biology, The Rockefeller University, New York, United States.ORCID 0000-0003-4831-4087
Isabel E WassingLaboratory of Chromosome and Cell Biology, The Rockefeller University, New York, United States.
Qingyuan JiaLaboratory of Chromosome and Cell Biology, The Rockefeller University, New York, United States.
Ji-Dung LuoBioinformatics Resource Center, The Rockefeller University, New York, United States.ORCID 0000-0003-0150-1440
Thomas CarrollBioinformatics Resource Center, The Rockefeller University, New York, United States.
Rockefeller University · US

Funding

Regulation of mitotic chromosomes - Revision - 2R35GM132111 · NIGMS · ROCKEFELLER UNIVERSITY · PI Hironori Funabiki · 2019 to 2026
$6.9M
NIGMS NIH HHS R35 GM132111
6 · The paper itself

Abstract

5-Methylcytosine (5mC) and DNA methyltransferases (DNMTs) are broadly conserved in eukaryotes but are also frequently lost during evolution. The mammalian SNF2 family ATPase HELLS and its plant ortholog DDM1 are critical for maintaining 5mC. Mutations in HELLS, its activator CDCA7, and the de novo DNA methyltransferase DNMT3B, cause immunodeficiency-centromeric instability-facial anomalies (ICF) syndrome, a genetic disorder associated with the loss of DNA methylation. We here examine the coevolution of CDCA7, HELLS and DNMTs. While DNMT3, the maintenance DNA methyltransferase DNMT1, HELLS, and CDCA7 are all highly conserved in vertebrates and green plants, they are frequently co-lost in other evolutionary clades. The presence-absence patterns of these genes are not random; almost all CDCA7 harboring eukaryote species also have HELLS and DNMT1 (or another maintenance methyltransferase, DNMT5). Coevolution of presence-absence patterns (CoPAP) analysis in Ecdysozoa further indicates coevolutionary linkages among CDCA7, HELLS, DNMT1 and its activator UHRF1. We hypothesize that CDCA7 becomes dispensable in species that lost HELLS or DNA methylation, and/or the loss of CDCA7 triggers the replacement of DNA methylation by other chromatin regulation mechanisms. Our study suggests that a unique specialized role of CDCA7 in HELLS-dependent DNA methylation maintenance is broadly inherited from the last eukaryotic common ancestor.

Indexed as

DNA MethylationNucleosomesAnimalsDNADNA (Cytosine-5-)-MethyltransferasesDNA HelicasesFaceMammalsPrimary Immunodeficiency DiseasesDNADNA (Cytosine-5-)-MethyltransferasesDNA HelicasesNucleosomescoevolutionDNA methylationevolutionary biologyICF syndromenonenucleosome remodeler

Identifiers

PMID37769127
PMCPMC10538959
OpenAlexW4379383094

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.