ArticleProceedings of the National Academy of Sciences of the United States of America2016
Strand-biased cytosine deamination at the replication fork causes cytosine to thymine mutations in Escherichia coli.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed, 101 citations in OpenAlex.
- Increased replication-associated single-stranded DNA promotes formaldehyde-induced mutagenesis.bioRxiv : the preprint server for biology · 2026Article
- On the origins and variation of nucleotide skews of archaeal genomes.Frontiers in microbiology · 2026Article
- APOBEC3A-Induced DNA Damage Drives Polymerase θ Dependency and Synthetic Lethality in Cancer.bioRxiv : the preprint server for biology · 2025Article
- Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe.Science advances · 2025Article
- The mutational landscape of Bacillus subtilis conditional hypermutators shows how proofreading skews DNA polymerase error rates.Nucleic acids research · 2025Article
- Defining APOBEC-induced mutation signatures and modifying activities in yeast.Methods in enzymology · 2025Article
- Clues to transcription/replication collision-induced DNA damage: it was RNAP, in the chromosome, with the fork.FEBS letters · 2025Review
- Differential effects on tumor progression by APOBEC3A, APOBEC3B, and APOBEC3H Haplotype I in a breast cancer mouse xenograft model.Frontiers in genetics · 2025Article
- Escherichia coli DNA replication: the old model organism still holds many surprises.FEMS microbiology reviews · 2024Review
- Origin, evolution, and maintenance of gene-strand bias in bacteria.Nucleic acids research · 2024Article
- Mesoscale DNA features impact APOBEC3A and APOBEC3B deaminase activity and shape tumor mutational landscapes.Nature communications · 2024Article
- Distinguishing preferences of human APOBEC3A and APOBEC3B for cytosines in hairpin loops, and reflection of these preferences in APOBEC-signature cancer genome mutations.Nature communications · 2024Article
- Mutation bias and adaptation in bacteria.Microbiology (Reading, England) · 2023Review
- APOBEC3B regulates R-loops and promotes transcription-associated mutagenesis in cancer.Nature genetics · 2023Article
- Genetic inhibitors of APOBEC3B-induced mutagenesis.Genome research · 2023Article
- Mechanistic insight into AP-endonuclease 1 cleavage of abasic sites at stalled replication fork mimics.Nucleic acids research · 2023Article
- The Effects of a High Concentration of Dissolved Oxygen on Actinobacteria from Lake Baikal.Metabolites · 2023Article
- Transcribed intergenic regions exhibit a lower frequency of nucleotide polymorphism than the untranscribed intergenic regions in the genomes ofJournal of genetics · 2023Article
- Strand asymmetries across genomic processes.Computational and structural biotechnology journal · 2023Review
- Competition for DNA binding between the genome protector replication protein A and the genome modifying APOBEC3 single-stranded DNA deaminases.Nucleic acids research · 2022Article
12 more citing papers are in PubMed but not listed here.
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6 authors at 2 institutions in 1 country.
Funding
Abstract
The rate of cytosine deamination is much higher in single-stranded DNA (ssDNA) than in double-stranded DNA, and copying the resulting uracils causes C to T mutations. To study this phenomenon, the catalytic domain of APOBEC3G (A3G-CTD), an ssDNA-specific cytosine deaminase, was expressed in an Escherichia coli strain defective in uracil repair (ung mutant), and the mutations that accumulated over thousands of generations were determined by whole-genome sequencing. C:G to T:A transitions dominated, with significantly more cytosines mutated to thymine in the lagging-strand template (LGST) than in the leading-strand template (LDST). This strand bias was present in both repair-defective and repair-proficient cells and was strongest and highly significant in cells expressing A3G-CTD. These results show that the LGST is accessible to cellular cytosine deaminating agents, explains the well-known GC skew in microbial genomes, and suggests the APOBEC3 family of mutators may target the LGST in the human genome.
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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.