ArticleThe Journal of experimental medicine2013
Changes in RNA polymerase II progression influence somatic hypermutation of Ig-related genes by AID.
Article in The Journal of experimental medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed.
- AID and TET2 cooperate to demethylate Irf4 for plasma cell fate in germinal center B cells.The Journal of experimental medicine · 2026Article
- DOT1L activity limits transcription elongation velocity and favors RNAPII pausing to facilitate mutagenesis by AID.Nature communications · 2026Article
- Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.Molecular cell · 2025Article
- Transcription elongation factor ELOF1 is required for efficient somatic hypermutation and class switch recombination.bioRxiv : the preprint server for biology · 2024Article
- Activation-induced cytidine deaminase an antibody diversification enzyme interacts with chromatin modifier UBN1 in B-cells.Scientific reports · 2023Article
- The IgHFrontiers in immunology · 2023Article
- Ig Enhancers Increase RNA Polymerase II Stalling at Somatic Hypermutation Target Sequences.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The role of HIRA-dependent H3.3 deposition and its modifications in the somatic hypermutation of immunoglobulin variable regions.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- 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
- Integrity of immunoglobulin variable regions is supported by GANP during AID-induced somatic hypermutation in germinal center B cells.International immunology · 2017Article
- Lingering Questions about Enhancer RNA and Enhancer Transcription-Coupled Genomic Instability.Trends in genetics : TIG · 2017Review
- Regulating infidelity: RNA-mediated recruitment of AID to DNA during class switch recombination.European journal of immunology · 2016Review
- RNA Exosome Regulates AID DNA Mutator Activity in the B Cell Genome.Advances in immunology · 2015Review
- IgH chain class switch recombination: mechanism and regulation.Journal of immunology (Baltimore, Md. : 1950) · 2014Review
- Spt5 accumulation at variable genes distinguishes somatic hypermutation in germinal center B cells from ex vivo-activated cells.The Journal of experimental medicine · 2014Article
- A source of the single-stranded DNA substrate for activation-induced deaminase during somatic hypermutation.Nature communications · 2014Article
- Generation and repair of AID-initiated DNA lesions in B lymphocytes.Frontiers of medicine · 2014Review
- Targeting of somatic hypermutation by immunoglobulin enhancer and enhancer-like sequences.PLoS biology · 2014Article
- Variations in brain DNA.Frontiers in aging neuroscience · 2014Review
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Authors and funding
5 authors.
Funding
Abstract
Somatic hypermutation (SHM) of Ig genes is initiated by the activation-induced cytidine deaminase (AID), and requires target gene transcription. We previously proposed that AID may associate with the RNA polymerase II (Pol). Here, to determine aspects of the transcription process required for SHM, we knocked-in a transcription terminator into an Ig gene variable region in DT40 chicken B cell line. We found that the human β-globin terminator was an efficient inhibitor of downstream transcription in these cells. The terminator reduced mutations downstream of the poly(A) signal, suggesting that the process of transcription is essential for efficient SHM and that AID has better access to its target when Pol is in the elongating rather than terminating mode. Mutations upstream of the poly(A) site were almost doubled in the active terminator clones compared with an inactivated terminator, and this region showed more single-stranded DNA, indicating that Pol pausing assists SHM. Moreover, the nontranscribed DNA strand was the preferred SHM target upstream of the active terminator. Pol pausing during poly(A) site recognition may facilitate persistence of negative supercoils, exposing the coding single strand and possibly allowing the nascent RNA intermittent reannealing with the template strand, for prolonged access of AID.
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