Evidence map›Paper›PMID 19901007›Full record

ArticleMutagenesis2010

Roles of Rev1, Pol zeta, Pol32 and Pol eta in the bypass of chromosomal abasic sites in Saccharomyces cerevisiae.

Paul A Auerbach, Bruce Demple

Open access · bronzeAbstract read
In one paragraph

Article in Mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

21 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. POLD3 as Controller of Replicative DNA Repair.International journal of molecular sciences · 2024
    Review
  4. Article
  5. The putative error prone polymerasenpj antimicrobials and resistance · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. DNA damage tolerance and a web of connections with DNA repair at Yale.The Yale journal of biology and medicine · 2013
    Article
  16. Article
  17. Review
  18. DNA polymerase delta in DNA replication and genome maintenance.Environmental and molecular mutagenesis · 2012
    Review
  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

2 authors at 1 institution in 1 country.

Paul A AuerbachDepartment of Genetics and Complex Diseases, Harvard School of Public Health, Boston, MA 02115, USA.
Bruce Demple
Harvard University · US

Funding

RADIATION BIOLOGY TRAINING PROGRAMT32CA009078 · NCI · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI D'ANDREA, ALAN D. · 1985 to 2009
$4.6M
HUMAN REPAIR ENZYME FOR 3-FRAGMENTS IN OXIDIZED DNAR01GM040000 · NIGMS · STATE UNIVERSITY NEW YORK STONY BROOK · PI DEMPLE, BRUCE F. · 1988 to 2010
$2.8M
NCI NIH HHS T32 CA009078NIGMS NIH HHS GM40000
6 · The paper itself

Abstract

Translesion synthesis (TLS) on DNA is a process by which potentially cytotoxic replication-blocking lesions are bypassed, but at the risk of increased mutagenesis. The exact in vivo role of the individual TLS enzymes in Saccharomyces cerevisiae has been difficult to determine from previous studies due to differing results from the variety of systems used. We have generated a series of S.cerevisiae strains in which each of the TLS-related genes REV1, REV3, REV7, RAD30 and POL32 was deleted, and in which chromosomal apyrimidinic sites were generated during normal cell growth by the activity of altered forms of human uracil-DNA glycosylase that remove undamaged cytosines or thymines. Deletion of REV1, REV3 or REV7 resulted in slower growth dependent on (rev3Delta and rev7Delta) or enhanced by (rev1Delta) expression of the mutator glycosylases and a nearly complete abolition of glycosylase-induced mutagenesis. Deletion of POL32 resulted in cell death when the mutator glycosylases were expressed and, in their absence, diminished spontaneous mutagenesis. RAD30 appeared to be unnecessary for mutagenesis in response to abasic sites, as deleting this gene caused no significant change in either the mutation rates or the mutational spectra due to glycosylase expression.

Indexed as

Base SequenceCell DeathDNA-Directed DNA PolymeraseDNA PrimersDNA ReplicationGene DeletionHumansMolecular Sequence DataMutagenesisNucleotidyltransferasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSequence Analysis, DNAUracil-DNA GlycosidaseY-Family DNA PolymerasesDNA-Directed DNA PolymeraseDNA PrimersNucleotidyltransferasesPol32 protein, S cerevisiaeREV1 protein, S cerevisiaeREV3 protein, S cerevisiaeREV7 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsUracil-DNA GlycosidaseY-Family DNA Polymerases

Identifiers

PMID19901007
PMCPMC2796187
OpenAlexW2118803767

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.