ArticleNucleic acids research2006
Sequence-dependent enhancement of hydrolytic deamination of cytosines in DNA by the restriction enzyme PspGI.
Article in Nucleic acids research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Nature communications · 2026Article
- Assessing the contribution of rare DNA states to cancer mutational signatures using sequence-specific conformational fingerprinting.Research square · 2025Article
- Article
- Efficient deamination of 5-methylcytosines in DNA by human APOBEC3A, but not by AID or APOBEC3G.Nucleic acids research · 2012Article
- Novel role of base excision repair in mediating cisplatin cytotoxicity.The Journal of biological chemistry · 2011Article
- Rotational position of a 5-methylcytosine-containing cyclobutane pyrimidine dimer in a nucleosome greatly affects its deamination rate.The Journal of biological chemistry · 2011Article
- Methyl CpG binding protein 2 (MeCP2) enhances photodimer formation at methyl-CpG sites but suppresses dimer deamination.Nucleic acids research · 2010Article
- Time-resolved fluorescence studies of nucleotide flipping by restriction enzymes.Nucleic acids research · 2009Article
- How PspGI, catalytic domain of EcoRII and Ecl18kI acquire specificities for different DNA targets.Nucleic acids research · 2008Article
- Central base pair flipping and discrimination by PspGI.Nucleic acids research · 2008Article
- DNA base flipping by both members of the PspGI restriction-modification system.Nucleic acids research · 2008Article
- The triple helix: 50 years later, the outcome.Nucleic acids research · 2008Review
- Chemical mapping of cytosines enzymatically flipped out of the DNA helix.Nucleic acids research · 2008Article
- Nucleotide flipping by restriction enzymes analyzed by 2-aminopurine steady-state fluorescence.Nucleic acids research · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hydrolytic deamination of cytosines in DNA creates uracil and, if unrepaired, these lesions result in C to T mutations. We have suggested previously that a possible way in which cells may prevent or reduce this chemical reaction is through the binding of proteins to DNA. We use a genetic reversion assay to show that a restriction enzyme, PspGI, protects cytosines within its cognate site, 5'-CCWGG (W is A or T), against deamination under conditions where no DNA cleavage can occur. It decreases the rate of cytosine deamination to uracil by 7-fold. However, the same protein dramatically increases the rate of deaminations within the site 5'-CCSGG (S is C or G) by approximately 15-fold. Furthermore, a similar increase in cytosine deaminations is also seen with a catalytically inactive mutant of the enzyme showing that endonucleolytic ability of the protein is dispensable for its mutagenic action. The sequences of the mutants generated in the presence of PspGI show that only one of the cytosines in CCSGG is predominantly converted to thymine. Our results are consistent with PspGI 'sensitizing' the cytosine in the central base pair in CCSGG for deamination. Remarkably, PspGI sensitizes this base for damage despite its inability to form stable complexes at CCSGG sites. These results can be explained if the enzyme has a transient interaction with this sequence during which it flips the central cytosine out of the helix. This prediction was validated by modeling the structure of PspGI-DNA complex based on the structure of the related enzyme Ecl18kI which is known to cause base-flipping.
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