Evidence map›Paper›PMID 19706533›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

The XNP remodeler targets dynamic chromatin in Drosophila.

Jonathan I Schneiderman, Akiko Sakai, Sara Goldstein, Kami Ahmad

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Multiple Roles of dXNP and dADD1-International journal of molecular sciences · 2023
    Review
  4. Article
  5. Reduced histone gene copy number disruptsbioRxiv : the preprint server for biology · 2023
    Article
  6. Article
  7. Article
  8. Article
  9. Mechanisms of Nucleosome Dynamics In Vivo.Cold Spring Harbor perspectives in medicine · 2016
    Review
  10. Article
  11. Article
  12. Replicating Nucleosomes.Science advances · 2015
    Article
  13. ATRX tolerates activity-dependent histone H3 methyl/phos switching to maintain repetitive element silencing in neurons.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  14. Article
  15. Histone variants and epigenetics.Cold Spring Harbor perspectives in biology · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Nucleosome-depleted chromatin gaps recruit assembly factors for the H3.3 histone variant.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Jonathan I SchneidermanDepartment of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA.
Akiko Sakai
Sara Goldstein
Kami Ahmad
Harvard University · US

Funding

Histone Variants and Transcription-linked DepositionR01GM068696 · NIGMS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI AHMAD, KAMRAN · 2004 to 2008
$1.6M
NIGMS NIH HHS R01 GM068696
6 · The paper itself

Abstract

Heterochromatic gene silencing results from the establishment of a repressive chromatin structure over reporter genes. Gene silencing is often variegated, implying that chromatin may stochastically switch from repressive to permissive structures as cells divide. To identify remodeling enzymes involved in reorganizing heterochromatin, we tested 11 SNF2-type chromatin remodelers in Drosophila for effects on gene silencing. Overexpression of five remodelers affects gene silencing, and the most potent de-repressor is the alpha-thalassaemia mental retardation syndrome X-linked (ATRX) homolog X-linked nuclear protein (XNP). Although the mammalian ATRX protein localizes to heterochromatin, Drosophila XNP is not a general component of heterochromatin. Instead, XNP localizes to active genes and to a major focus near the heterochromatin of the X chromosome. The XNP focus corresponds to an unusual decondensed satellite DNA block, and both active genes and the XNP focus are sites of ongoing nucleosome replacement. We suggest that the XNP remodeler modulates nucleosome dynamics at its target sites to limit chromatin accessibility. Although XNP at active genes may contribute to gene silencing, we find that a single focus is present across Drosophila species and that perturbation of this site cripples heterochromatic gene silencing. Thus, the XNP focus appears to be a functional genetic element that can contribute to gene silencing throughout the nucleus.

Indexed as

AnimalsAnimals, Genetically ModifiedCell NucleusChromatinChromatin Assembly and DisassemblyChromosome MappingDNA HelicasesDrosophilaDrosophila melanogasterDrosophila ProteinsEyeFemaleGene Expression Regulation, DevelopmentalGene SilencingGreen Fluorescent ProteinsHeterochromatinChromatinDNA HelicasesDrosophila ProteinsGreen Fluorescent ProteinsHeterochromatinNucleosomesXNP protein, Drosophila

Identifiers

PMID19706533
PMCPMC2725014
OpenAlexW2039256261

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.