Evidence map›Paper›PMID 36991495›Full record

ArticleCell & bioscience2023

H3K27me3-H3K4me1 transition at bivalent promoters instructs lineage specification in development.

Yue Yu, Xinjie Li, Rui Jiao, Yang Lu, Xuan Jiang, Xin Li

Open access · goldAbstract read
In one paragraph

Article in Cell & bioscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Epigenetic remodeling during early embryonic development.Frontiers in cell and developmental biology · 2026
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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

6 authors at 1 institution in 1 country.

Yue Yu *School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Xinjie Li *School of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Rui JiaoThe Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Yang LuSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China.
Xuan JiangSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China. jiangx79@mail.sysu.edu.cn.
Xin LiSchool of Medicine, Shenzhen Campus of Sun Yat-sen University, Shenzhen, China. lixin253@mail.sysu.edu.cn.ORCID http://orcid.org/0000-0001-8328-4894
Sun Yat-sen University · CN

Funding

Guangzhou Municipal Science and Technology Project 201904010007Innovative Research Group Project of the National Natural Science Foundation of China 81872299Shenzhen Science and Technology Innovation Program JCYJ20190807160011600Shenzhen Science and Technology Innovation Program JCYJ20210324124808023
6 · The paper itself

Abstract

backgroundBivalent genes, of which promoters are marked by both H3K4me3 (trimethylation of histone H3 on lysine 4) and H3K27me3 (trimethylation of histone H3 on lysine 27), play critical roles in development and tumorigenesis. Monomethylation on lysine 4 of histone H3 (H3K4me1) is commonly associated with enhancers, but H3K4me1 is also present at promoter regions as an active bimodal or a repressed unimodal pattern. Whether the co-occurrence of H3K4me1 and bivalent marks at promoters plays regulatory role in development is largely unknown.

resultsWe report that in the process of lineage differentiation, bivalent promoters undergo H3K27me3-H3K4me1 transition, the loss of H3K27me3 accompanies by bimodal pattern loss or unimodal pattern enrichment of H3K4me1. More importantly, this transition regulates tissue-specific gene expression to orchestrate the development. Furthermore, knockout of Eed (Embryonic Ectoderm Development) or Suz12 (Suppressor of Zeste 12) in mESCs (mouse embryonic stem cells), the core components of Polycomb repressive complex 2 (PRC2) which catalyzes H3K27 trimethylation, generates an artificial H3K27me3-H3K4me1 transition at partial bivalent promoters, which leads to up-regulation of meso-endoderm related genes and down-regulation of ectoderm related genes, thus could explain the observed neural ectoderm differentiation failure upon retinoic acid (RA) induction. Finally, we find that lysine-specific demethylase 1 (LSD1) interacts with PRC2 and contributes to the H3K27me3-H3K4me1 transition in mESCs.

conclusionsThese findings suggest that H3K27me3-H3K4me1 transition plays a key role in lineage differentiation by regulating the expression of tissue specific genes, and H3K4me1 pattern in bivalent promoters could be modulated by LSD1 via interacting with PRC2.

Indexed as

Bivalent promoterH3K27me3-H3K4me1 transitionLSD1Neural ectoderm differentiationTissue-specific genes

Identifiers

PMID36991495
PMCPMC10061859
OpenAlexW4361290424

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.