ArticleThe Journal of experimental medicine2005
The very 5' end and the constant region of Ig genes are spared from somatic mutation because AID does not access these regions.
Article in The Journal of experimental medicine, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 63 citations in OpenAlex.
- Article
- Article
- A Bayesian model based computational analysis of the relationship between bisulfite accessible single-stranded DNA in chromatin and somatic hypermutation of immunoglobulin genes.PLoS computational biology · 2021Article
- Role of Dot1L and H3K79 methylation in regulating somatic hypermutation of immunoglobulin genes.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Analysis of Somatic Hypermutation in the JH4 intron of Germinal Center B cells from Mouse Peyer's Patches.Journal of visualized experiments : JoVE · 2021Article
- AID in Chronic Lymphocytic Leukemia: Induction and Action During Disease Progression.Frontiers in oncology · 2021Review
- Characterization of DNA G-Quadruplex Structures in Human Immunoglobulin Heavy Variable (IGHV) Genes.Frontiers in immunology · 2021Article
- AID-RNA polymerase II transcription-dependent deamination of IgV DNA.Nucleic acids research · 2019Article
- Diversity in the Cow Ultralong CDR H3 Antibody Repertoire.Frontiers in immunology · 2018Review
- Bcl6 Is Required for Somatic Hypermutation and Gene Conversion in Chicken DT40 Cells.PloS one · 2016Article
- BCR repertoire sequencing: different patterns of B-cell activation after two Meningococcal vaccines.Immunology and cell biology · 2015Article
- A source of the single-stranded DNA substrate for activation-induced deaminase during somatic hypermutation.Nature communications · 2014Article
- 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
- Does DNA repair occur during somatic hypermutation?Seminars in immunology · 2012Review
- Negative supercoiling creates single-stranded patches of DNA that are substrates for AID-mediated mutagenesis.PLoS genetics · 2012Article
- Article
- AID: a riddle wrapped in a mystery inside an enigma.Immunologic research · 2011Review
- Article
- Error-prone DNA repair activity during somatic hypermutation in shark B lymphocytes.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Somatic hypermutation (SHM) is restricted to VDJ regions and their adjacent flanks in immunoglobulin (Ig) genes, whereas constant regions are spared. Mutations occur after about 100 nucleotides downstream of the promoter and extend to 1-2 kb. We have asked why the very 5' and most of the 3' region of Ig genes are unmutated. Does the activation-induced cytosine deaminase (AID) that initiates SHM not gain access to these regions, or does AID gain access, but the resulting uracils are repaired error-free because error-prone repair does not gain access? The distribution of mutations was compared between uracil DNA glycosylase (Ung)-deficient and wild-type mice in endogenous Ig genes and in an Ig transgene. If AID gains access to the 5' and 3' regions that are unmutated in wild-type mice, one would expect an "AID footprint," namely transition mutations from C and G in Ung-deficient mice in the regions normally devoid of SHM. We find that the distribution of total mutations and transitions from C and G is indistinguishable in wild-type and Ung-deficient mice. Thus, AID does not gain access to the 5' and constant regions of Ig genes. The implications for the role of transcription and Ung in SHM are discussed.
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