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Article

Colon cancer-associated mutator DNA polymerase δ variant causes expansion of dNTP pools increasing its own infidelity.

Proceedings of the National Academy of Sciences of the United States of America - 12 May 2015

Mertz Tony M, Sharma Sushma, Chabes Andrei, Shcherbakova Polina V

Abstract excerpt

Defects in DNA polymerases δ (Polδ) and ε (Polε) cause hereditary colorectal cancer and have been implicated in the etiology of some sporadic colorectal and endometrial tumors. We previously reported that the yeast pol3-R696W allele mimicking a human cancer-associated variant, POLD1-R689W, causes a catastrophic increase in spontaneous mutagenesis. Here, we describe the mechanism of this extraordinary mutator...

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Share to Chromosomes
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 25827231
DOI: 10.1073/pnas.1422934112
PMCID: PMC4434702

Genes

POLD1

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Colon cancer-associated mutator DNA polymerase δ variant causes expansion of dNTP pools increasing its own infidelity.PMID 25827231Read ↗

dNTP pool levels modulate mutator phenotypes of error-prone DNA polymerase ε variants.Semantic proximity Read ↗

Enhanced polymerase activity permits efficient synthesis by cancer-associated DNA polymerase ϵ variants at low dNTP levels.Semantic proximity Read ↗

Nucleotide selectivity defect and mutator phenotype conferred by a colon cancer-associated DNA polymerase δ mutation in human cells.Semantic proximity Read ↗

A cancer-associated DNA polymerase delta variant modeled in yeast causes a catastrophic increase in genomic instability.Semantic proximity Read ↗

Endogenous DNA replication stress results in expansion of dNTP pools and a mutator phenotype.Semantic proximity Read ↗

Explosive mutation accumulation triggered by heterozygous human Pol ε proofreading-deficiency is driven by suppression of mismatch repairSemantic proximity Read ↗

Mutagenic mechanisms of cancer-associated DNA polymerase ε allelesSemantic proximity Read ↗

Mutagenic mechanisms of cancer-associated DNA polymerase ϵ alleles.Semantic proximity Read ↗

A common cancer-associated DNA polymerase ε mutation causes an exceptionally strong mutator phenotype, indicating fidelity defects distinct from loss of proofreading.Semantic proximity Read ↗

A substitution in the fingers domain of DNA polymerase δ reduces fidelity by altering nucleotide discrimination in the catalytic site.Semantic proximity Read ↗

Increased rates of genomic deletions generated by mutations in the yeast gene encoding DNA polymerase delta or by decreases in the cellular levels of DNA polymerase delta.Semantic proximity Read ↗

Human Pol ε-dependent replication errors and the influence of mismatch repair on their correction.Semantic proximity Read ↗

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