ArticleProceedings of the National Academy of Sciences of the United States of America2005
Complex regulation of somatic hypermutation by cis-acting sequences in the endogenous IgH gene in hybridoma cells.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- The IgHFrontiers in immunology · 2023Article
- Targeting of somatic hypermutation by immunoglobulin enhancer and enhancer-like sequences.PLoS biology · 2014Article
- AID and Apobec3G haphazard deamination and mutational diversity.Cellular and molecular life sciences : CMLS · 2013Review
- Article
- The zebrafish IgH locus contains multiple transcriptional regulatory regions.Developmental and comparative immunology · 2011Article
- Comparison of identical and functional Igh alleles reveals a nonessential role for Eμ in somatic hypermutation and class-switch recombination.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Requirement for enhancer specificity in immunoglobulin heavy chain locus regulation.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- In a model of immunoglobulin heavy-chain (IGH)/MYC translocation, the Igh 3' regulatory region induces MYC expression at the immature stage of B cell development.Genes, chromosomes & cancer · 2007Article
- Forced expression of AID facilitates the isolation of class switch variants from hybridoma cells.Journal of immunological methods · 2006Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
To create high-affinity antibodies, B cells target a high rate of somatic hypermutation (SHM) to the Ig variable-region genes that encode the antigen-binding site. This mutational process requires transcription and is triggered by activation-induced cytidine deaminase (AID), which converts deoxycytidine to deoxyuridine. Mistargeting of AID to non-Ig genes is thought to result in the malignant transformation of B cells, but the mechanism responsible for targeting SHM to certain DNA regions and not to others is largely unknown. Cis-acting elements have been proposed to play a role in directing the hypermutation machinery, but the motifs required for targeting SHM have been difficult to identify because many of the candidate elements, such as promoters or enhancers, are also required for transcription of Ig genes. Here we describe a system in cultured hybridoma cells in which transcription of the endogenous heavy-chain Ig gene continues in the absence of the core intronic enhancer (Emu) and its flanking matrix attachment regions (MARs). When AID is expressed in these cells, SHM occurred at the WT frequency even when Emu and the MARs were absent together. Interestingly, SHM occurred at less than the WT frequency when Emu or the MARs were individually absent. Our results suggest that these intronic regulatory elements can exert a complex influence on SHM that is separable from their role in regulating transcription.
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