Evidence map›Paper›PMID 19178722›Full record

ArticleEpigenetics & chromatin2009

High-resolution mapping of heterochromatin redistribution in a Drosophila position-effect variegation model.

Maartje J Vogel, Ludo Pagie, Wendy Talhout, Marja Nieuwland, Ron M Kerkhoven, Bas van Steensel

Open access · goldAbstract read
In one paragraph

Article in Epigenetics & chromatin, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Live analysis of position-effect variegation inProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  8. Exact breakpoints of themicroPublication biology · 2022
    Article
  9. Article
  10. Review
  11. Evolution and Diversification ofFrontiers in plant science · 2019
    Article
  12. Review
  13. Generalized nucleation and looping model for epigenetic memory of histone modifications.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  14. Article
  15. Article
  16. Article
  17. Human inversions and their functional consequences.Briefings in functional genomics · 2015
    Review
  18. Review
  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

6 authors at 2 institutions in 1 country.

Maartje J VogelDivision of Gene Regulation, Netherlands Cancer Institute, Plesmanlaan 121, 1066CX Amsterdam, The Netherlands. maartje.vogel@gmail.com
Ludo Pagie
Wendy Talhout
Marja Nieuwland
Ron M Kerkhoven
Bas van Steensel
The Netherlands Cancer Institute · NLOncode Institute · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPosition-effect variegation (PEV) is the stochastic transcriptional silencing of a gene positioned adjacent to heterochromatin. white-mottled X-chromosomal inversions in Drosophila are classic PEV models that show variegation of the eye color gene white due to its relocation next to pericentric heterochromatin. It has been suggested that in these models the spreading of heterochromatin across the rearrangement breakpoint causes the silencing of white. However, the extent of this spreading and the precise pattern of heterochromatin redistribution have remained unclear. To obtain insight into the mechanism of PEV, we constructed high-resolution binding maps of Heterochromatin Protein 1 (HP1) on white-mottled chromosomes.

resultsWe find that HP1 invades euchromatin across the inversion breakpoints over approximately 175 kb and approximately 30 kb, causing de novo association of HP1 with 20 genes. However, HP1 binding levels in these regions show substantial local variation, and white is the most strongly bound gene. Remarkably, white is also the only gene that is detectably repressed by heterochromatin. Furthermore, we find that HP1 binding to the invaded region is particularly sensitive to the dosage of the histone methyltransferase Su(var)3-9, indicating that the de novo formed heterochromatin is less stable than naturally occurring constitutive heterochromatin.

conclusionOur molecular maps demonstrate that heterochromatin can invade a normally euchromatic region, yet the strength of HP1 binding and effects on gene expression are highly dependent on local context. Our data suggest that the white gene has an unusual intrinsic affinity for heterochromatin, which may cause this gene to be more sensitive to PEV than most other genes.

Identifiers

PMID19178722
PMCPMC2644302
OpenAlexW2025537241

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.