Evidence map›Paper›PMID 26492073›Full record

ArticlePLoS genetics2015

Mre11 and Blm-Dependent Formation of ALT-Like Telomeres in Ku-Deficient Ustilago maydis.

Eun Young Yu, José Pérez-Martín, William K Holloman, Neal F Lue

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. 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
0.8field-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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Global Gene Expression of Post-Senescent Telomerase-NegativeJournal of fungi (Basel, Switzerland) · 2023
    Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
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  14. Article
  15. Article
  16. Article
  17. Single telomere length analysis inMicrobial cell (Graz, Austria) · 2018
    Article
  18. Article
  19. Review
  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

4 authors at 3 institutions in 2 countries.

Eun Young YuDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Medical College of Cornell University, New York, New York, United States of America.
José Pérez-MartínInstituto de Biología Funcional y Genómica CSIC, Salamanca, Spain.
William K HollomanDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Medical College of Cornell University, New York, New York, United States of America; Sandra and Edward Meyer Cancer Center, Weill Cornell Medical College, New York, New York, United States of America.
Neal F LueDepartment of Microbiology & Immunology, W. R. Hearst Microbiology Research Center, Weill Medical College of Cornell University, New York, New York, United States of America; Sandra and Edward Meyer Cancer Center, Weill Cornell Medical College, New York, New York, United States of America.
Cornell University · USHearst (United States) · USInstituto de Biología Funcional y Genómica · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A subset of human cancer cells uses a specialized, aberrant recombination pathway known as ALT to maintain telomeres, which in these cells are characterized by complex aberrations including length heterogeneity, high levels of unpaired C-strand, and accumulation of extra-chromosomal telomere repeats (ECTR). These phenotypes have not been recapitulated in any standard budding or fission yeast mutant. We found that eliminating Ku70 or Ku80 in the yeast-like fungus Ustilago maydis results initially in all the characteristic telomere aberrations of ALT cancer cells, including C-circles, a highly specific marker of ALT. Subsequently the ku mutants experience permanent G2 cell cycle arrest, accompanied by loss of telomere repeats from chromosome ends and even more drastic accumulation of very short ECTRs (vsECTRs). The deletion of atr1 or chk1 rescued the lethality of the ku mutant, and "trapped" the telomere aberrations in the early ALT-like stage. Telomere abnormalities are telomerase-independent, but dramatically suppressed by deletion of mre11 or blm, suggesting major roles for these factors in the induction of the ALT pathway. In contrast, removal of other DNA damage response and repair factors such as Rad51 has disparate effects on the ALT phenotypes, suggesting that these factors process ALT intermediates or products. Notably, the antagonism of Ku and Mre11 in the induction of ALT is reminiscent of their roles in DSB resection, in which Blm is also known to play a key role. We suggest that an aberrant resection reaction may constitute an early trigger for ALT telomeres, and that the outcomes of ALT are distinct from DSB because of the unique telomere nucleoprotein structure.

Indexed as

Recombination, GeneticAntigens, NuclearCell ProliferationChromosomesDNA-Binding ProteinsDNA DamageDNA RepairG2 Phase Cell Cycle CheckpointsHumansKu AutoantigenRad51 RecombinaseRecQ HelicasesTelomeraseTelomereUstilagoAntigens, NuclearBloom syndrome proteinDNA-Binding ProteinsKu AutoantigenRad51 RecombinaseRecQ HelicasesTelomeraseXrcc6 protein, human

Identifiers

PMID26492073
PMCPMC4619612
OpenAlexW1895295080

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Registered trials

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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.