Evidence map›Paper›PMID 7681584›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1993

In vivo evidence for endogenous DNA alkylation damage as a source of spontaneous mutation in eukaryotic cells.

W Xiao, L Samson

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

63 citing papers in PubMed, 183 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Tools and systems for evolutionary engineering of biomolecules and microorganisms.Journal of industrial microbiology & biotechnology · 2019
    Review
  11. The abundant DNA adductThe Journal of biological chemistry · 2019
    Article
  12. Review
  13. The capacity of oocytes for DNA repair.Cellular and molecular life sciences : CMLS · 2018
    Review
  14. Article
  15. Article
  16. Inflammasomes in Inflammation-Induced Cancer.Frontiers in immunology · 2017
    Review
  17. ThreeFrontiers in plant science · 2016
    Article
  18. Article
  19. Article
  20. DNA damage to a single chromosome end delays anaphase onset.The Journal of biological chemistry · 2014
    Article

3 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.

W XiaoDepartment of Molecular and Cellular Toxicology, Harvard School of Public Health, Boston, MA 02115.
L Samson
Harvard University · US

Funding

EUKARYTIC DNA ALKYLATION REPAIRR01CA055042 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1991 to 2010
$4.8M
NCI NIH HHS CA55042
6 · The paper itself

Abstract

Three genes that participate in the repair of DNA alkylation damage were recently cloned from Saccharomyces cerevisiae: the MGT1 O6-methylguanine DNA methyltransferase gene, the MAG 3-methyladenine DNA glycosylase gene, and the APN1 apurinic/apyrimidinic (AP) endonuclease gene. Altering the expression levels of these three genes produced significant changes in the S. cerevisiae spontaneous mutation rate. Spontaneous mutation increased in the absence of the MGT1 DNA methyltransferase, presumably because unrepaired, spontaneously produced, O6-alkylguanine lesions mispair during replication. Moreover, changing the ratios of the MAG 3-methyladenine DNA glycosylase and the APN1 AP endonuclease had profound effects on spontaneous mutation rates. In the absence of APN1, the overexpression of MAG increased spontaneous mutation, and the underexpression of MAG decreased spontaneous mutation. We infer that the MAG glycosylase acts upon spontaneously produced 3-alkyladenine and 7-alkylguanine DNA lesions to produce mutagenic abasic sites, and that if the repair of these abasic sites is not initiated by the APN1 AP endonuclease they cause mutations during replication. Our results indicate that eukaryotic cells harbor endogenous metabolites that alkylate nuclear DNA at both oxygens and nitrogens.

Indexed as

DNA DamageDNA GlycosylasesGenes, FungalMutationAlkylationDeoxyribonuclease IV (Phage T4-Induced)DNA-(Apurinic or Apyrimidinic Site) LyaseDNA, FungalDNA RepairEndodeoxyribonucleasesGene ExpressionKineticsMethyl MethanesulfonateMethylnitronitrosoguanidineMethyltransferasesN-Glycosyl Hydrolases3-methyladenine-DNA glycosylaseDeoxyribonuclease IV (Phage T4-Induced)DNA-(Apurinic or Apyrimidinic Site) LyaseDNA, FungalDNA GlycosylasesEndodeoxyribonucleasesMethyl MethanesulfonateMethylnitronitrosoguanidineMethyltransferasesN-Glycosyl HydrolasesO(6)-Methylguanine-DNA Methyltransferase

Identifiers

PMID7681584
PMCPMC46036
OpenAlexW2059852484

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.