Evidence map›Paper›PMID 16203987›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Drosophila ATM and ATR checkpoint kinases control partially redundant pathways for telomere maintenance.

Xiaolin Bi, Deepa Srikanta, Laura Fanti, Sergio Pimpinelli, RamaKrishna Badugu, Rebecca Kellum, Yikang S Rong

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

55 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Telomere Checkpoint in Development and Aging.International journal of molecular sciences · 2023
    Review
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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

7 authors at 2 institutions in 1 country.

Xiaolin BiLaboratory of Molecular Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Deepa Srikanta
Laura Fanti
Sergio Pimpinelli
RamaKrishna Badugu
Rebecca Kellum
Yikang S Rong
National Institutes of Health · USUniversity of Kentucky · US

Funding

DNA Double Strand Break Repair in Drosophila MelanogasterZ01BC010446 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI RONG, YIKANG · 2002 to 2008
$1.9M
DISSECTION OF HETEROCHROMATIN ASSEMBLY IN DROSOPHILAR01GM059765 · NIGMS · UNIVERSITY OF KENTUCKY · PI KELLUM, REBECCA · 1999 to 2002
$669k
Intramural NIH HHSNIGMS NIH HHS GM059765NIGMS NIH HHS R01 GM059765
6 · The paper itself

Abstract

In higher eukaryotes, the ataxia telangiectasia mutated (ATM) and ATM and Rad3-related (ATR) checkpoint kinases play distinct, but partially overlapping, roles in DNA damage response. Yet their interrelated function has not been defined for telomere maintenance. We discover in Drosophila that the two proteins control partially redundant pathways for telomere protection: the loss of ATM leads to the fusion of some telomeres, whereas the loss of both ATM and ATR renders all telomeres susceptible to fusion. The ATM-controlled pathway includes the Mre11 and Nijmegen breakage syndrome complex but not the Chk2 kinase, whereas the ATR-regulated pathway includes its partner ATR-interacting protein but not the Chk1 kinase. This finding suggests that ATM and ATR regulate different molecular events at the telomeres compared with the sites of DNA damage. This compensatory relationship between ATM and ATR is remarkably similar to that observed in yeast despite the fact that the biochemistry of telomere elongation is completely different in the two model systems. We provide evidence suggesting that both the loading of telomere capping proteins and normal telomeric silencing requires ATM and ATR in Drosophila and propose that ATM and ATR protect telomere integrity by safeguarding chromatin architecture that favors the loading of telomere-elongating, capping, and silencing proteins.

Indexed as

Drosophila melanogasterAnimalsAnimals, Genetically ModifiedAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA DamageDNA Repair EnzymesDrosophila ProteinsEndodeoxyribonucleasesFemaleGene SilencingMaleProtein Serine-Threonine KinasesRecombinant Fusion ProteinsTelomereAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA-Binding ProteinsDNA Repair EnzymesDrosophila ProteinsEndodeoxyribonucleasesMei-41 protein, DrosophilaMre11 protein, DrosophilaProtein Serine-Threonine KinasesRecombinant Fusion ProteinsTumor Suppressor Proteins

Identifiers

PMID16203987
PMCPMC1257705
OpenAlexW2106640045

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.