Evidence map›Paper›PMID 35137160›Full record

ArticleNucleic acids research2022

Loss of histone methyltransferase SETD1B in oogenesis results in the redistribution of genomic histone 3 lysine 4 trimethylation.

Courtney W Hanna, Jiahao Huang, Christian Belton, Susanne Reinhardt, Andreas Dahl, Simon Andrews, A Francis Stewart, Andrea Kranz, Gavin Kelsey

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Ketogenic Diet as an Epigenetic Therapy in SETD1B-Related Epilepsy.Annals of clinical and translational neurology · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Journal of developmental biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Role of H3K4 monomethylation in gene regulation.Current opinion in genetics & development · 2024
    Review
  16. Article
  17. Review
  18. Epigenetic factor competition reshapes the EMT landscape.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  19. Article
  20. 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

9 authors at 4 institutions in 2 countries.

Courtney W HannaEpigenetics Programme, Babraham Institute, Cambridge, UK.
Jiahao HuangEpigenetics Programme, Babraham Institute, Cambridge, UK.
Christian BeltonEpigenetics Programme, Babraham Institute, Cambridge, UK.
Susanne ReinhardtDresden Concept Genome Center, Center for Molecular and Cellular Bioengineering, Biotechnology Center, Technische Universität Dresden, 01307, Germany.
Andreas DahlDresden Concept Genome Center, Center for Molecular and Cellular Bioengineering, Biotechnology Center, Technische Universität Dresden, 01307, Germany.
Simon AndrewsBioinformatics Group, Babraham Institute, Cambridge CB22 3AT, UK.
A Francis StewartGenomics, Center for Molecular and Cellular Bioengineering, Biotechnology Center, Technische Universität Dresden, 01307, Germany.
Andrea KranzGenomics, Center for Molecular and Cellular Bioengineering, Biotechnology Center, Technische Universität Dresden, 01307, Germany.
Gavin KelseyEpigenetics Programme, Babraham Institute, Cambridge, UK.ORCID 0000-0002-9762-5634
Babraham Institute · GBCenter for Systems Biology Dresden · DEMax Planck Institut für Zellbiologie · DETechnische Universität Dresden · DE

Funding

Biotechnology and Biological Sciences Research Council BBS/E/B/000C0423Medical Research Council MR/K011332/1Medical Research Council MR/S000437/1
6 · The paper itself

Abstract

Histone 3 lysine 4 trimethylation (H3K4me3) is an epigenetic mark found at gene promoters and CpG islands. H3K4me3 is essential for mammalian development, yet mechanisms underlying its genomic targeting are poorly understood. H3K4me3 methyltransferases SETD1B and MLL2 (KMT2B) are essential for oogenesis. We investigated changes in H3K4me3 in Setd1b conditional knockout (cKO) oocytes using ultra-low input ChIP-seq, with comparisons to DNA methylation and gene expression analyses. H3K4me3 was redistributed in Setd1b cKO oocytes showing losses at active gene promoters associated with downregulated gene expression. Remarkably, many regions also gained H3K4me3, in particular those that were DNA hypomethylated, transcriptionally inactive and CpG-rich, which are hallmarks of MLL2 targets. Consequently, loss of SETD1B disrupts the balance between MLL2 and de novo DNA methyltransferases in determining the epigenetic landscape during oogenesis. Our work reveals two distinct, complementary mechanisms of genomic targeting of H3K4me3 in oogenesis, with SETD1B linked to gene expression and MLL2 to CpG content.

Indexed as

HistonesLysineAnimalsCpG IslandsDNA MethylationHistone MethyltransferasesMammalsOogenesisHistone MethyltransferasesHistonesLysine

Identifiers

PMID35137160
PMCPMC8887468
OpenAlexW4210660131

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.