Evidence map›Paper›PMID 31320637›Full record

ArticleNature communications2019

Activation of neuronal genes via LINE-1 elements upon global DNA demethylation in human neural progenitors.

Marie E Jönsson, Per Ludvik Brattås, Charlotte Gustafsson, Rebecca Petri, David Yudovich, Karolina Pircs, Shana Verschuere, Sofia Madsen, Jenny Hansson, Jonas Larsson and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 113 citations in OpenAlex.

  1. Review
  2. Article
  3. Conserved SINE and lineage-variable LINE-1 depletion at neurodevelopmental disorder promoters.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Article
  4. LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. ATRX: From Chromatin Remodeling to Disease.Genesis (New York, N.Y. : 2000) · 2025
    Review
  13. Article
  14. Review
  15. From the genome's perspective: Bearing somatic retrotransposition to leverage the regulatory potential of L1 RNAs.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

15 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

13 authors at 3 institutions in 2 countries.

Marie E JönssonWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden.
Per Ludvik BrattåsWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden.
Charlotte GustafssonCenter for Hematology and Regenerative Medicine Huddinge, Karolinska Institute, 141 52, Stockholm, Sweden.
Rebecca PetriWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden.
David YudovichDivision of Molecular Medicine and Gene Therapy, Department of Laboratory Medicine and Lund Stem Cell Center, BMC A12, Lund University, 221 84, Lund, Sweden.
Karolina PircsWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden.
Shana VerschuereWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden.
Sofia MadsenWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden.
Jenny HanssonLaboratory of Proteomic Hematology, Department of Laboratory Medicine and Lund Stem Cell Center, BMC B12, Lund University, 221 84, Lund, Sweden.ORCID http://orcid.org/0000-0001-9174-8089
Jonas LarssonDivision of Molecular Medicine and Gene Therapy, Department of Laboratory Medicine and Lund Stem Cell Center, BMC A12, Lund University, 221 84, Lund, Sweden.
Robert MånssonCenter for Hematology and Regenerative Medicine Huddinge, Karolinska Institute, 141 52, Stockholm, Sweden.
Alexander MeissnerDepartment of Genome Regulation, Max Planck Institute for Molecular Genetics, 14195, Berlin, Germany.
Johan JakobssonWallenberg Neuroscience Center and Lund Stem Cell Center, Laboratory of Molecular Neurogenetics, Department of Experimental Medical Science, BMC A11, Lund University, 221 84, Lund, Sweden. johan.jakobsson@med.lu.se.ORCID http://orcid.org/0000-0003-0669-7673
Lund University · SEKarolinska Institutet · SEMax Planck Institute for Molecular Genetics · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA methylation contributes to the maintenance of genomic integrity in somatic cells, in part through the silencing of transposable elements. In this study, we use CRISPR-Cas9 technology to delete DNMT1, the DNA methyltransferase key for DNA methylation maintenance, in human neural progenitor cells (hNPCs). We observe that inactivation of DNMT1 in hNPCs results in viable, proliferating cells despite a global loss of DNA CpG-methylation. DNA demethylation leads to specific transcriptional activation and chromatin remodeling of evolutionarily young, hominoid-specific LINE-1 elements (L1s), while older L1s and other classes of transposable elements remain silent. The activated L1s act as alternative promoters for many protein-coding genes involved in neuronal functions, revealing a hominoid-specific L1-based transcriptional network controlled by DNA methylation that influences neuronal protein-coding genes. Our results provide mechanistic insight into the role of DNA methylation in silencing transposable elements in somatic human cells, as well as further implicating L1s in human brain development and disease.

Indexed as

DNA DemethylationBrainChromatin Assembly and DisassemblyCpG IslandsCRISPR-Cas SystemsDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationGene SilencingHumansLong Interspersed Nucleotide ElementsNeural Stem CellsTranscriptional ActivationDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, human

Identifiers

PMID31320637
PMCPMC6639357
OpenAlexW2960183779

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.