ArticleGenome research2017
APOBEC3A/B-induced mutagenesis is responsible for 20% of heritable mutations in the TpCpW context.
Article in Genome research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Break-induced replication forms long mutable single-strand DNA during meiosis.Nature communications · 2026Article
- Mutational Signatures in Wild Type Escherichia coli Strains Reveal Predominance of DNA Polymerase Errors.Genome biology and evolution · 2024Article
- Unusual mammalian usage of TGA stop codons reveals that sequence conservation need not imply purifying selection.PLoS biology · 2022Article
- Spectrum of DNA mismatch repair failures viewed through the lens of cancer genomics and implications for therapy.Clinical science (London, England : 1979) · 2022Article
- Population sequencing data reveal a compendium of mutational processes in the human germ line.Science (New York, N.Y.) · 2021Article
- Effect ofAmerican journal of cancer research · 2021Article
- Whole-genome sequencing of 508 patients identifies key molecular features associated with poor prognosis in esophageal squamous cell carcinoma.Cell research · 2020Article
- Nucleosome positioning stability is a modulator of germline mutation rate variation across the human genome.Nature communications · 2020Article
- Germline variants and somatic mutation signatures of breast cancer across populations of African and European ancestry in the US and Nigeria.International journal of cancer · 2019Article
- Error-prone bypass of DNA lesions during lagging-strand replication is a common source of germline and cancer mutations.Nature genetics · 2019Article
- Strategy of Human Cytomegalovirus To Escape Interferon Beta-Induced APOBEC3G Editing Activity.Journal of virology · 2018Article
- Human mismatch repair system balances mutation rates between strands by removing more mismatches from the lagging strand.Genome research · 2017Article
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3 authors.
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Abstract
APOBEC3A/B cytidine deaminase is responsible for the majority of cancerous mutations in a large fraction of cancer samples. However, its role in heritable mutagenesis remains very poorly understood. Recent studies have demonstrated that both in yeast and in human cancerous cells, most APOBEC3A/B-induced mutations occur on the lagging strand during replication and on the nontemplate strand of transcribed regions. Here, we use data on rare human polymorphisms, interspecies divergence, and de novo mutations to study germline mutagenesis and to analyze mutations at nucleotide contexts prone to attack by APOBEC3A/B. We show that such mutations occur preferentially on the lagging strand and on nontemplate strands of transcribed regions. Moreover, we demonstrate that APOBEC3A/B-like mutations tend to produce strand-coordinated clusters, which are also biased toward the lagging strand. Finally, we show that the mutation rate is increased 3' of C→G mutations to a greater extent than 3' of C→T mutations, suggesting pervasive trans-lesion bypass of the APOBEC3A/B-induced damage. Our study demonstrates that 20% of C→T and C→G mutations in the TpCpW context-where W denotes A or T, segregating as polymorphisms in human population-or 1.4% of all heritable mutations are attributable to APOBEC3A/B activity.
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