Evidence map›Paper›PMID 11333215›Full record

ArticleGenetics2001

Repair of topoisomerase-mediated DNA damage in bacteriophage T4.

B A Stohr, K N Kreuzer

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. DNA- and DNA-Protein-Crosslink Repair in Plants.International journal of molecular sciences · 2019
    Review
  5. Mechanisms of DNA-protein crosslink repair.Nature reviews. Molecular cell biology · 2017
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Endonuclease cleavage of blocked replication forks: An indirect pathway of DNA damage from antitumor drug-topoisomerase complexes.Proceedings of the National Academy of Sciences of the United States of America · 2003
    Article
  12. Bacteriophage T4 genome.Microbiology and molecular biology reviews : MMBR · 2003
    Review
  13. Article
  14. Article
  15. The tight linkage between DNA replication and double-strand break repair in bacteriophage T4.Proceedings of the National Academy of Sciences of the United States of America · 2001
    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

2 authors at 2 institutions in 1 country.

B A StohrDepartments of Microbiology and Biochemistry, Duke University Medical Center, Durham, NC 27710, USA.
K N Kreuzer
Duke Medical Center · USDuke University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007171 · NIGMS · DUKE UNIVERSITY · PI KONTOS, CHRISTOPHER D · 1985 to 2021
$31.2M
ANTITUMOR AGENTS AND THE BACTERIOPHAGE T4 TOPOISOMERASER01CA060836 · NCI · DUKE UNIVERSITY · PI KREUZER, KENNETH N · 1993 to 2001
$505k
NCI NIH HHS CA60836NIGMS NIH HHS T32-GM07171-26
6 · The paper itself

Abstract

Type II topoisomerase inhibitors are used to treat both tumors and bacterial infections. These inhibitors stabilize covalent DNA-topoisomerase cleavage complexes that ultimately cause lethal DNA damage. A functional recombinational repair apparatus decreases sensitivity to these drugs, suggesting that topoisomerase-mediated DNA damage is amenable to such repair. Using a bacteriophage T4 model system, we have developed a novel in vivo plasmid-based assay that allows physical analysis of the repair products from one particular topoisomerase cleavage site. We show that the antitumor agent 4'-(9-acridinylamino)methanesulphon-m-anisidide (m-AMSA) stabilizes the T4 type II topoisomerase at the strong topoisomerase cleavage site on the plasmid, thereby stimulating recombinational repair. The resulting m-AMSA-dependent repair products do not form in the absence of functional topoisomerase and appear at lower drug concentrations with a drug-hypersensitive topoisomerase mutant. The appearance of repair products requires that the plasmid contain a T4 origin of replication. Finally, genetic analyses demonstrate that repair product formation is absolutely dependent on genes 32 and 46, largely dependent on genes uvsX and uvsY, and only partly dependent on gene 49. Very similar genetic requirements are observed for repair of endonuclease-generated double-strand breaks, suggesting mechanistic similarity between the two repair pathways.

Indexed as

DNA DamageDNA RepairAmsacrineBacteriophage T4Base SequenceDNA PrimersDNA Topoisomerases, Type IIDNA, ViralMutationPlasmidsRecombination, GeneticAmsacrineDNA PrimersDNA Topoisomerases, Type IIDNA, Viral

Identifiers

PMID11333215
PMCPMC1461630
OpenAlexW2123505368

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.