Evidence map›Paper›PMID 30861354›Full record

ArticleEpigenetics2019

The chromatin remodeling protein Lsh alters nucleosome occupancy at putative enhancers and modulates binding of lineage specific transcription factors.

Jianke Ren, Richard Finney, Kai Ni, Maggie Cam, Kathrin Muegge

Open access · hybridAbstract read
In one paragraph

Article in Epigenetics, 2019. 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
2.1field-weighted citation impact, top 13% 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, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. The DNA-helicase HELLS drives ALKCell death & disease · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Lsh/HELLS is required for B lymphocyte development and immunoglobulin class switch recombination.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  18. Article
  19. Review
  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

5 authors at 4 institutions in 1 country.

Jianke Rena Mouse Cancer Genetics Program , National Cancer Institute , Frederick , MD , USA.
Richard Finneyb CCR Collaborative Bioinformatics Resource , Center for Cancer Research, National Cancer Institute , Bethesda , MD , USA.
Kai Nia Mouse Cancer Genetics Program , National Cancer Institute , Frederick , MD , USA.
Maggie Camb CCR Collaborative Bioinformatics Resource , Center for Cancer Research, National Cancer Institute , Bethesda , MD , USA.
Kathrin Mueggea Mouse Cancer Genetics Program , National Cancer Institute , Frederick , MD , USA.
Center for Cancer Research · USCancer Genetics (United States) · USLeidos (United States) · USNational Cancer Institute · US

Funding

CCR NIH HHS HHSN261200800001CNCI NIH HHS HHSN261200800001E
6 · The paper itself

Abstract

Dynamic regulation of chromatin accessibility is a key feature of cellular differentiation during embryogenesis, but the precise factors that control access to chromatin remain largely unknown. Lsh/HELLS is critical for normal development and mutations of Lsh in human cause the ICF (Immune deficiency, Centromeric instability, Facial anomalies) syndrome, a severe immune disorder with multiple organ deficiencies. We report here that Lsh, previously known to regulate DNA methylation level, has a genome wide chromatin remodeling function. Using micrococcal nuclease (MNase)-seq analysis, we demonstrate that Lsh protects MNase accessibility at transcriptional regulatory regions characterized by DNase I hypersensitivity and certain histone 3 (H3) tail modifications associated with enhancers. Using an auxin-inducible degron system, allowing proteolytical degradation of Lsh, we show that Lsh mediated changes in nucleosome occupancy are independent of DNA methylation level and are characterized by reduced H3 occupancy. While Lsh mediated nucleosome occupancy prevents binding sites for transcription factors in wild type cells, depletion of Lsh leads to an increase in binding of ectopically expressed tissue specific transcription factors to their respective binding sites. Our data suggests that Lsh mediated chromatin remodeling can modulate nucleosome positioning at a subset of putative enhancers contributing to the preservation of cellular identity through regulation of accessibility.

Indexed as

Enhancer Elements, GeneticAnimalsBinding SitesChromatin Assembly and DisassemblyDNA HelicasesDNA MethylationHistone CodeMice, KnockoutMicrococcal NucleaseNucleosomesRegulatory Sequences, Nucleic AcidTranscription FactorsDNA Helicaseslymphoid specific helicase, mouseMicrococcal NucleaseNucleosomesTranscription Factorschromatin accessLshMNasenucleosome occupancytranscription factor

Identifiers

PMID30861354
PMCPMC6557562
OpenAlexW2921833140

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.