Evidence map›Paper›PMID 16957771›Full record

ArticleThe EMBO journal2006

A novel function of DNA polymerase zeta regulated by PCNA.

Matthew R Northam, Parie Garg, Dmitri M Baitin, Peter M J Burgers, Polina V Shcherbakova

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

68 citing papers in PubMed, 100 citations in OpenAlex.

  1. Structural and Mechanistic Diversity of Constitutional Chromoanagenesis.Methods in molecular biology (Clifton, N.J.) · 2025
    Article
  2. eLife · 2024
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  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Making Choices: DNA Replication Fork Recovery Mechanisms.Seminars in cell & developmental biology · 2021
    Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. GC content elevates mutation and recombination rates in the yeastProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  20. Review

8 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

5 authors at 2 institutions in 1 country.

Matthew R NorthamEppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Parie Garg
Dmitri M Baitin
Peter M J Burgers
Polina V Shcherbakova
University of Nebraska Medical Center · USWashington University in St. Louis · US

Funding

ENZYMOLOGY OF REPLICATION OF YEAST CHROMOSOMAL DNAR01GM032431 · NIGMS · WASHINGTON UNIVERSITY · PI BURGERS, PETER M · 1985 to 2015
$6.5M
Role of DNA polymerases in chromosome stability controlK22ES011644 · NIEHS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SHCHERBAKOVA, POLINA V · 2003 to 2005
$321k
NIEHS NIH HHS 5 K22 ES011644NIEHS NIH HHS K22 ES011644NIGMS NIH HHS GM32431NIGMS NIH HHS R01 GM032431
6 · The paper itself

Abstract

DNA polymerase zeta (Polzeta) participates in translesion DNA synthesis and is involved in the generation of the majority of mutations induced by DNA damage. The mechanisms that license access of Polzeta to the primer terminus and regulate the extent of its participation in genome replication are poorly understood. The Polzeta-dependent damage-induced mutagenesis requires monoubiquitination of proliferating cell nuclear antigen (PCNA) that is triggered by exposure to mutagens. We show that Polzeta contributes to DNA replication and causes mutagenesis not only in response to DNA damage but also in response to malfunction of normal replicative machinery due to mutations in replication genes. These replication defects lead to ubiquitination of PCNA even in the absence of DNA damage. Unlike damage-induced mutagenesis, the Polzeta-dependent spontaneous mutagenesis in replication mutants is reduced in strains defective in both ubiquitination and sumoylation of Lys164 of PCNA. Additionally, studies of a PCNA mutant defective for functional interactions with Polzeta, but not for monoubiquitination by the Rad6/Rad18 complex demonstrate a role for PCNA in regulating the mutagenic activity of Polzeta separate from its modification at Lys164.

Indexed as

Base SequenceDNA DamageDNA-Directed DNA PolymeraseDNA, FungalDNA ReplicationGenes, FungalMutationPhenotypeProliferating Cell Nuclear AntigenSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSmall Ubiquitin-Related Modifier ProteinsUbiquitinUltraviolet RaysDNA-Directed DNA PolymeraseDNA, FungalDNA polymerase zetaProliferating Cell Nuclear AntigenSaccharomyces cerevisiae ProteinsSmall Ubiquitin-Related Modifier ProteinsUbiquitin

Identifiers

PMID16957771
PMCPMC1570441
OpenAlexW2130937328

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.