Evidence map›Paper›PMID 33024290›Full record

ReviewNature reviews. Genetics2021

Active turnover of DNA methylation during cell fate decisions.

Aled Parry, Steffen Rulands, Wolf Reik

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing 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

124 citing papers in PubMed.

  1. Review
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  11. Review
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  15. Review
  16. Review
  17. Article
  18. Review
  19. TET3 protects theiScience · 2025
    Article
  20. Article

64 more citing papers are in PubMed but not listed here.

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

3 authors.

Aled ParryEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, UK. aled.parry@babraham.ac.uk.ORCID http://orcid.org/0000-0001-5192-3727
Steffen RulandsMax Planck Institute for the Physics of Complex Systems, Dresden, Germany.ORCID http://orcid.org/0000-0001-6398-1553
Wolf ReikEpigenetics Programme, The Babraham Institute, Babraham Research Campus, Cambridge, UK. wolf.reik@babraham.ac.uk.ORCID http://orcid.org/0000-0003-0216-9881

Funding

Biotechnology and Biological Sciences Research Council BB/K010867/1Wellcome Trust 095645/Z/11/ZWellcome Trust 215912/Z/19/Z
6 · The paper itself

Abstract

DNA methylation is a key layer of epigenetic regulation. The deposition of methylation marks relies on the catalytic activity of DNA methyltransferases (DNMTs), and their active removal relies on the activity of ten-eleven translocation (TET) enzymes. Paradoxically, in important biological contexts these antagonistic factors are co-expressed and target overlapping genomic regions. The ensuing cyclic biochemistry of cytosine modifications gives rise to a continuous, out-of-thermal equilibrium transition through different methylation states. But what is the purpose of this intriguing turnover of DNA methylation? Recent evidence demonstrates that methylation turnover is enriched at gene distal regulatory elements, including enhancers, and can give rise to large-scale oscillatory dynamics. We discuss this phenomenon and propose that DNA methylation turnover might facilitate key lineage decisions.

Indexed as

DNA MethylationEpigenesis, GeneticCell LineageCytosineDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesHumansMixed Function OxygenasesProto-Oncogene ProteinsCytosineDioxygenasesDNA-Binding ProteinsDNA (Cytosine-5-)-MethyltransferasesMixed Function OxygenasesProto-Oncogene ProteinsTET1 protein, humanTET2 protein, human

Identifiers

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.