ArticleMolecular and cellular biology2005
Targeting of the activation-induced cytosine deaminase is strongly influenced by the sequence and structure of the targeted DNA.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 56 citations in OpenAlex.
- Histone H3.3 promotes IgV gene diversification by enhancing formation of AID-accessible single-stranded DNA.The EMBO journal · 2016Article
- Activation-induced deoxycytidine deaminase (AID) co-transcriptional scanning at single-molecule resolution.Nature communications · 2015Article
- A mathematical model for scanning and catalysis on single-stranded DNA, illustrated with activation-induced deoxycytidine deaminase.The Journal of biological chemistry · 2013Article
- AID and Apobec3G haphazard deamination and mutational diversity.Cellular and molecular life sciences : CMLS · 2013Review
- Changes in RNA polymerase II progression influence somatic hypermutation of Ig-related genes by AID.The Journal of experimental medicine · 2013Article
- AIDing antibody diversity by error-prone mismatch repair.Seminars in immunology · 2012Review
- Stabilised DNA secondary structures with increasing transcription localise hypermutable bases for somatic hypermutation in IGHV3-23.Immunogenetics · 2012Article
- Nucleosome stability dramatically impacts the targeting of somatic hypermutation.Molecular and cellular biology · 2012Article
- Analysis of a single-stranded DNA-scanning process in which activation-induced deoxycytidine deaminase (AID) deaminates C to U haphazardly and inefficiently to ensure mutational diversity.The Journal of biological chemistry · 2011Article
- Article
- The pattern of somatic hypermutation of Ig genes is altered when p53 is inactivated.Molecular immunology · 2010Article
- Regulation of activation-induced cytidine deaminase DNA deamination activity in B-cells by Ser38 phosphorylation.Biochemical Society transactions · 2009Article
- The activation-induced cytidine deaminase (AID) efficiently targets DNA in nucleosomes but only during transcription.The Journal of experimental medicine · 2009Article
- Interference of mismatch and base excision repair during the processing of adjacent U/G mispairs may play a key role in somatic hypermutation.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
- Post-translational regulation of activation-induced cytidine deaminase.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Review
- Immunoglobulin class switch recombination: study through human natural mutants.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2009Article
- Transcriptional pausing and stalling causes multiple clustered mutations by human activation-induced deaminase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2009Article
- Hypermutation at A/T sites during G.U mismatch repair in vitro by human B-cell lysates.The Journal of biological chemistry · 2008Article
- Impact of phosphorylation and phosphorylation-null mutants on the activity and deamination specificity of activation-induced cytidine deaminase.The Journal of biological chemistry · 2008Article
- Mechanism and regulation of class switch recombination.Annual review of immunology · 2008Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Activation-induced deaminase (AID) initiates immunoglobulin somatic hypermutation (SHM). Since in vitro AID was shown to deaminate cytosines on single-stranded DNA or the nontranscribed strand, it remained a puzzle how in vivo AID targets both DNA strands equally. Here we investigate the roles of transcription and DNA sequence in cytosine deamination. Strikingly different results are found with different substrates. Depending on the target sequence, the transcribed DNA strand is targeted as well as or better than the nontranscribed strand. The preferential targeting is not related to the frequency of AID hot spots. Comparison of cytosine deamination by AID and bisulfite shows different targeting patterns suggesting that AID may locally unwind the DNA. We conclude that somatic hypermutation on both DNA strands is the natural outcome of AID action on a transcribed gene; furthermore, the DNA sequence or structure and topology play major roles in targeting AID in vitro and in vivo. On the other hand, the lack of mutations in the first approximately 100 nucleotides and beyond about 1 to 2 kb from the promoter of immunoglobulin genes during SHM must be due to special conditions of transcription and chromatin in vivo.
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Registered trials
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.