Evidence map›Paper›PMID 15713803›Full record

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

Abrupt disruption of capping and a single source for recombinationally elongated telomeres in Kluyveromyces lactis.

Zeki Topcu, Kristy Nickles, Charity Davis, Michael J McEachern

Abstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. The many facets of homologous recombination at telomeres.Microbial cell (Graz, Austria) · 2015
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Telomeric circles: universal players in telomere maintenance?Nature structural & molecular biology · 2009
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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 2 institutions in 1 country.

Zeki TopcuDepartment of Genetics, University of Georgia, Fred C. Davison Life Sciences Complex, Athens, GA 30602, USA.
Kristy Nickles
Charity Davis
Michael J McEachern
Massachusetts Institute of Technology · USUniversity of Georgia · US

Funding

RECOMBINATIONAL TELOMERE MAINTENANCER01GM061645 · NIGMS · UNIVERSITY OF GEORGIA (UGA) · PI MCEACHERN, MICHAEL J. · 2000 to 2010
$2.2M
NIGMS NIH HHS GM61645-01NIGMS NIH HHS R01 GM061645
6 · The paper itself

Abstract

Eukaryotic cells, including some human cancers, that lack telomerase can sometimes maintain telomeres by using recombination. It was recently proposed that recombinational telomere elongation (RTE) in a telomerase-deletion mutant of the yeast Kluyveromyces lactis occurs through a roll-and-spread mechanism as described in our previous work. According to this model, a tiny circle of telomeric DNA is copied by a rolling-circle mechanism to generate one long telomere, the sequence of which is then spread to all other telomeres by gene-conversion events. In support of this model, we demonstrate here that RTE in K. lactis occurs by amplification of a sequence originating from a single telomere. When a mutationally tagged telomere is of normal length, its sequence is spread to all other telomeres at a frequency (approximately 10%) consistent with random selection among the 12 telomeres in the cell. However, when the mutationally tagged telomere is considerably longer than other telomeres, cellular senescence is partially suppressed, and the sequence of the tagged telomere is spread to all other telomeres in >90% of cells. Strikingly, the transition between a state resistant to recombination and a state capable of initiating recombination is abrupt, typically occurring when telomeres are approximately 3-4 repeats long. Last, we show that mutant repeats that are defective at regulating telomerase are also defective at regulating telomere length during RTE.

Indexed as

Recombination, GeneticTelomereBase SequenceDNA PrimersKluyveromycesDNA Primers

Identifiers

PMID15713803
PMCPMC552925
OpenAlexW2046313094

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.