Hypothesis: Somatic hypermutation by gene conversion via the error prone DNA→RNA→DNA information loop

1987 ◽  
Vol 24 (6) ◽  
pp. 667-673 ◽  
Author(s):  
E.J. Steele ◽  
J.W. Pollard
Keyword(s):  
Gene Conversion ◽  
Somatic Hypermutation

scholarly journals Bcl6 Is Required for Somatic Hypermutation and Gene Conversion in Chicken DT40 Cells

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0149146 ◽  
Author(s):  
Alan M. Williams ◽  
Yaakov Maman ◽  
Jukka Alinikula ◽  
David G. Schatz
Keyword(s):  
Gene Conversion ◽  
Somatic Hypermutation ◽  
Dt40 Cells

scholarly journals Brca1 in immunoglobulin gene conversion and somatic hypermutation

DNA Repair ◽  
2008 ◽  
Vol 7 (2) ◽  
pp. 253-266 ◽  
Author(s):  
Simonne Longerich ◽  
Brian J. Orelli ◽  
Richard W. Martin ◽  
Douglas K. Bishop ◽  
Ursula Storb
Keyword(s):  
Gene Conversion ◽  
Somatic Hypermutation ◽  
Immunoglobulin Gene

scholarly journals AID Mediates Hypermutation by Deaminating Single Stranded DNA

2003 ◽  
Vol 197 (10) ◽  
pp. 1291-1296 ◽  
Author(s):  
Sarah K. Dickerson ◽  
Eleonora Market ◽  
Eva Besmer ◽  
F. Nina Papavasiliou
Keyword(s):  
Gene Conversion ◽  
Somatic Hypermutation ◽  
Class Switch Recombination ◽  
Functional Link ◽  
Single Stranded Dna ◽  
Class Switch ◽  
Mutational Hotspots ◽  
Activation Induced Deaminase ◽  
Precise Role

Activation-induced deaminase (AID) is a protein indispensable for the diversification of immunoglobulin (Ig) genes by somatic hypermutation (SHM), class switch recombination (CSR), and gene conversion. To date, the precise role of AID in these processes has not been determined. Here we demonstrate that purified, tetrameric AID can deaminate cytidine residues in DNA, but not in RNA. Furthermore, we show that AID will bind and deaminate only single-stranded DNA, which implies a direct, functional link between hypermutation and transcription. Finally, AID does not target mutational hotspots, thus mutational targeting to specific residues must be attributed to different factors.

scholarly journals Control of gene conversion and somatic hypermutation by immunoglobulin promoter and enhancer sequences

2006 ◽  
Vol 203 (13) ◽  
pp. 2919-2928 ◽  
Author(s):  
Shu Yuan Yang ◽  
Sebastian D. Fugmann ◽  
David G. Schatz
Keyword(s):  
Rna Polymerase Ii ◽  
Gene Conversion ◽  
Transcriptional Control ◽  
Somatic Hypermutation ◽  
Cytidine Deaminase ◽  
Cis Acting ◽  
Gene Diversification ◽  
Combined Action ◽  
High Level ◽  
Enhancer Sequences

It is thought that gene conversion (GCV) and somatic hypermutation (SHM) of immunoglobulin (Ig) genes occur in two steps: the generation of uracils in DNA by activation-induced cytidine deaminase, followed by their subsequent repair by various DNA repair pathways to generate sequence-diversified products. It is not known how either of the two steps is targeted specifically to Ig loci. Because of the tight link between transcription and SHM, we have investigated the role of endogenous Ig light chain (IgL) transcriptional control elements in GCV/SHM in the chicken B cell line DT40. Promoter substitution experiments led to identification of a strong RNA polymerase II promoter incapable of supporting efficient GCV/SHM. This surprising finding indicates that high levels of transcription are not sufficient for robust GCV/SHM in Ig loci. Deletion of the IgL enhancer in a context in which high-level transcription was not compromised showed that the enhancer is not necessary for GCV/SHM. Our results indicate that cis-acting elements are important for Ig gene diversification, and we propose that targeting specificity is achieved through the combined action of several Ig locus elements that include the promoter.

Ablation of XRCC2/3 transforms immunoglobulin V gene conversion into somatic hypermutation

Nature ◽  
2001 ◽  
Vol 412 (6850) ◽  
pp. 921-926 ◽  
Author(s):  
Julian E. Sale ◽  
Daniella M. Calandrini ◽  
Minoru Takata ◽  
Shunichi Takeda ◽  
Michael S. Neuberger
Keyword(s):  
Gene Conversion ◽  
Somatic Hypermutation ◽  
V Gene
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