Evidence map›Paper›PMID 18845840›Full record

ArticleGenetics2008

Loss of the histone variant H2A.Z restores capping to checkpoint-defective telomeres in Drosophila.

Yikang S Rong

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.7field-weighted citation impact, top 29% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. In thebioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. TheG3 (Bethesda, Md.) · 2018
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. One identity or more for telomeres?Frontiers in oncology · 2013
    Article
  11. Article
  12. Article
  13. 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

1 author at 1 institution in 1 country.

Yikang S RongLaboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA. rongy@mail.nih.gov
National Institutes of Health · US

Funding

DNA Double Strand Break Repair in Drosophila MelanogasterZIABC010446 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RONG, YIKANG · 2009 to 2015
$6.9M
DNA Double Strand Break Repair in Drosophila MelanogasterZ01BC010446 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RONG, YIKANG · 2002 to 2008
$1.9M
Intramural NIH HHS
6 · The paper itself

Abstract

The conserved histone variant H2A.Z fulfills many functions by being an integral part of the nucleosomes placed at specific regions of the genome. Telomeres cap natural ends of chromosomes to prevent their recognition as double-strand breaks. At yeast telomeres, H2A.Z prevents the spreading of silent chromatin into proximal euchromatin. A role for H2A.Z in capping, however, has not been reported in any organism. Here, I uncover such a role for Drosophila H2A.Z. Loss of H2A.Z, through mutations in either its gene or the domino gene for the Swr1 chromatin-remodeling protein, suppressed the fusion of telomeres that lacked the protection of checkpoint proteins: ATM, ATR, and the Mre11-Rad50-NBS complex. Loss of H2A.Z partially restores the loading of the HOAP capping protein, possibly accounting for the partial restoration in capping. I propose that, in the absence of H2A.Z, checkpoint-defective telomeres adopt alternative structures, which are permissive for the loading of the capping machinery at Drosophila telomeres.

Indexed as

AnimalsDrosophilaGenes, cdcHistonesMutationTelomereHistones

Identifiers

PMID18845840
PMCPMC2600928
OpenAlexW2062009551

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.