Evidence map›Paper›PMID 34782763›Full record

ArticleNature genetics2021

A cis-acting mechanism mediates transcriptional memory at Polycomb target genes in mammals.

Daniel Holoch, Michel Wassef, Cecilia Lövkvist, Dina Zielinski, Setareh Aflaki, Bérangère Lombard, Tiphaine Héry, Damarys Loew, Martin Howard, Raphaël Margueron

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Nature genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.9field-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

47 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Stochastic modeling of epigenetic memory.NPJ systems biology and applications · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Polycomb function in early mouse development.Cell death and differentiation · 2025
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 4 countries.

Daniel Holoch *Institut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.
Michel Wassef *Institut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.
Cecilia LövkvistJohn Innes Centre, Norwich Research Park, Norwich, UK. cecilia.loevkvist@bric.ku.dk.ORCID http://orcid.org/0000-0001-7696-7814
Dina ZielinskiInstitut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.ORCID http://orcid.org/0000-0002-6188-9590
Setareh AflakiInstitut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.
Bérangère LombardInstitut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.
Tiphaine HéryInstitut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.
Damarys LoewInstitut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France.ORCID http://orcid.org/0000-0002-9111-8842
Martin HowardJohn Innes Centre, Norwich Research Park, Norwich, UK.ORCID http://orcid.org/0000-0001-7670-0781
Raphaël MargueronInstitut Curie, Paris Sciences et Lettres Research University, Sorbonne University, Paris, France. raphael.margueron@curie.fr.ORCID http://orcid.org/0000-0002-9093-7977
Centre National de la Recherche Scientifique · FRJohn Innes Centre · GBUniversité Paris Sciences et Lettres · FR

Funding

Biotechnology and Biological Sciences Research Council BBS/E/J/000PR9773
6 · The paper itself

Abstract

Epigenetic inheritance of gene expression states enables a single genome to maintain distinct cellular identities. How histone modifications contribute to this process remains unclear. Using global chromatin perturbations and local, time-controlled modulation of transcription, we establish the existence of epigenetic memory of transcriptional activation for genes that can be silenced by the Polycomb group. This property emerges during cell differentiation and allows genes to be stably switched after a transient transcriptional stimulus. This transcriptional memory state at Polycomb targets operates in cis; however, rather than relying solely on read-and-write propagation of histone modifications, the memory is also linked to the strength of activating inputs opposing Polycomb proteins, and therefore varies with the cellular context. Our data and computational simulations suggest a model whereby transcriptional memory arises from double-negative feedback between Polycomb-mediated silencing and active transcription. Transcriptional memory at Polycomb targets thus depends not only on histone modifications but also on the gene-regulatory network and underlying identity of a cell.

Indexed as

Epigenesis, GeneticTranscriptional ActivationAnimalsFemaleHistone CodeHumansMaleMammalsMicePolycomb-Group ProteinsPolycomb Repressive Complex 2Polycomb-Group ProteinsPolycomb Repressive Complex 2

Identifiers

PMID34782763
OpenAlexW3212913189

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.