Evidence map›Paper›PMID 9799256›Full record

ArticleGenetics1998

Chromosome break-induced DNA replication leads to nonreciprocal translocations and telomere capture.

G Bosco, J E Haber

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

121 citing papers in PubMed, 218 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  5. Article
  6. POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Host translesion polymerases are required for viral genome integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  13. Article
  14. Role and Regulation of Pif1 Family Helicases at the Replication Fork.International journal of molecular sciences · 2022
    Review
  15. Mechanistic origins of diverse genome rearrangements in cancer.Seminars in cell & developmental biology · 2022
    Review
  16. Article
  17. Break-induced replication mechanisms in yeast and mammals.Current opinion in genetics & development · 2021
    Review
  18. Repair of DNA Breaks by Break-Induced Replication.Annual review of biochemistry · 2021
    Review
  19. Article
  20. Article

61 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

2 authors at 1 institution in 1 country.

G BoscoRosenstiel Center and Department of Biology, Brandeis University, Waltham, Massachusetts 02454-9110, USA.
J E Haber
Brandeis University · US

Funding

Recombination Mechanisms in Yeast Cell DifferentiationR37GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2007 to 2016
$5.5M
RECOMBINATION MECHANISMS IN YEAST CELL DIFFERENTIATIONR01GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 1985 to 2006
$3.4M
NIGMS NIH HHS GM20056
6 · The paper itself

Abstract

In yeast, broken chromosomes can be repaired by recombination, resulting in nonreciprocal translocations. In haploid cells suffering an HO endonuclease-induced, double-strand break (DSB), nearly 2% of the broken chromosome ends recombined with a sequence near the opposite chromosome end, which shares only 72 bp of homology with the cut sequence. This produced a repaired chromosome with the same 20-kb sequence at each end. Diploid strains were constructed in which the broken chromosome shared homology with the unbroken chromosome only on the centromere-proximal side of the DSB. More than half of these cells repaired the DSB by copying sequences distal to the break from the unbroken template chromosome. All these events were RAD52 dependent. Pedigree analysis established that DSBs occurring in G1 were repaired by a replicative mechanism, producing two identical daughter cells. We discuss the implications of these data in understanding telomerase-independent replication of telomeres, gene amplification, and the evolution of chromosomal ends.

Indexed as

DNA ReplicationTranslocation, GeneticChromosomes, FungalDNA, FungalGene Expression Regulation, FungalSaccharomyces cerevisiaeTelomereDNA, Fungal

Identifiers

PMID9799256
PMCPMC1460379
OpenAlexW2129755545

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.