Evidence map›Paper›PMID 10224249›Full record

ArticleGenetics1999

RAD50 and RAD51 define two pathways that collaborate to maintain telomeres in the absence of telomerase.

S Le, J K Moore, J E Haber, C W Greider

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 217 papers.

0numbers the graph read from it
0cells of the map it votes in
217citing papers in PubMed
16.0field-weighted citation impact, top 1% 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

217 citing papers in PubMed, 401 citations in OpenAlex.

  1. Article
  2. Article
  3. Fission yeast RPA-TERT-Tpz1bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Inverse-folding design of yeast telomerase RNA increases activitybioRxiv : the preprint server for biology · 2023
    Article

157 more citing papers are in PubMed but not listed here.

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.

S LeDepartment of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
J K Moore
J E Haber
C W Greider
Brandeis University · USJohns Hopkins Medicine · US

Funding

TRANSPOSITION OF TN7P01CA016519 · NCI · JOHNS HOPKINS UNIVERSITY · PI BEACHY, PHILIP A · 1985 to 2010
$21.4M
TETRAHYMENA TELOMERASE RNPR01GM043080 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREIDER, CAROL W · 1990 to 2011
$4.3M
TELOMERASE INHIBITION IN HUMAN IMMORTALIZED CELLSF32CA068736 · NCI · JOHNS HOPKINS UNIVERSITY · PI LE, SIYUAN · 1995 to 1998
–
NCI NIH HHS CA16519NCI NIH HHS CA 68736NIGMS NIH HHS GM43080
6 · The paper itself

Abstract

Telomere length is maintained by the de novo addition of telomere repeats by telomerase, yet recombination can elongate telomeres in the absence of telomerase. When the yeast telomerase RNA component, TLC1, is deleted, telomeres shorten and most cells die. However, gene conversion mediated by the RAD52 pathway allows telomere lengthening in rare survivor cells. To further investigate the role of recombination in telomere maintenance, we assayed telomere length and the ability to generate survivors in several isogenic DNA recombination mutants, including rad50, rad51, rad52, rad54, rad57, xrs2, and mre11. The rad51, rad52, rad54, and rad57 mutations increased the rate of cell death in the absence of TLC1. In contrast, although the rad50, xrs2, and mre11 strains initially had short telomeres, double mutants with tlc1 did not affect the rate of cell death, and survivors were generated at later times than tlc1 alone. While none of the double mutants of recombination genes and tlc1 (except rad52 tlc1) blocked the ability to generate survivors, a rad50 rad51 tlc1 triple mutant did not allow the generation of survivors. Thus RAD50 and RAD51 define two separate pathways that collaborate to allow cells to survive in the absence of telomerase.

Indexed as

EndodeoxyribonucleasesExodeoxyribonucleasesSaccharomyces cerevisiae ProteinsAdenosine TriphosphatasesBlotting, SouthernCell DivisionCell SurvivalDNA-Binding ProteinsDNA HelicasesDNA Repair EnzymesEpistasis, GeneticFungal ProteinsGenotypeMutagenesisRad51 RecombinaseRad52 DNA Repair and Recombination ProteinAdenosine TriphosphatasesDNA-Binding ProteinsDNA HelicasesDNA Repair EnzymesEndodeoxyribonucleasesExodeoxyribonucleasesFungal ProteinsMRE11 protein, S cerevisiaeRAD50 protein, S cerevisiaeRAD51 protein, S cerevisiaeRad51 RecombinaseRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeRAD54 protein, S cerevisiaeRAD57 protein, S cerevisiaeRNA, FungalSaccharomyces cerevisiae ProteinsTelomeraseXRS2 protein, S cerevisiae

Identifiers

PMID10224249
PMCPMC1460580
OpenAlexW2141288561

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.