ArticleThe Journal of experimental medicine2004
Examination of Msh6- and Msh3-deficient mice in class switching reveals overlapping and distinct roles of MutS homologues in antibody diversification.
Article in The Journal of experimental medicine, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 95 citations in OpenAlex.
- B cell class switch recombination is regulated by DYRK1A through MSH6 phosphorylation.Nature communications · 2023Article
- A Human MSH6 Germline Variant Associated With Systemic Lupus Erythematosus Induces Lupus-like Disease in Mice.ACR open rheumatology · 2022Article
- AID function in somatic hypermutation and class switch recombination.Acta biochimica et biophysica Sinica · 2022Review
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- The Complex Interplay between DNA Injury and Repair in Enzymatically Induced Mutagenesis and DNA Damage in B Lymphocytes.International journal of molecular sciences · 2017Review
- Non-canonical uracil processing in DNA gives rise to double-strand breaks and deletions: relevance to class switch recombination.Nucleic acids research · 2016Article
- Antibody diversification caused by disrupted mismatch repair and promiscuous DNA polymerases.DNA repair · 2016Review
- Individual substitution mutations in the AID C terminus that ablate IgH class switch recombination.PloS one · 2015Article
- Mismatch repair proteins and AID activity are required for the dominant negative function of C-terminally deleted AID in class switching.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Article
- Fanca deficiency reduces A/T transitions in somatic hypermutation and alters class switch recombination junctions in mouse B cells.The Journal of experimental medicine · 2014Article
- AID and Apobec3G haphazard deamination and mutational diversity.Cellular and molecular life sciences : CMLS · 2013Review
- MSH6- or PMS2-deficiency causes re-replication in DT40 B cells, but it has little effect on immunoglobulin gene conversion or on repair of AID-generated uracils.Nucleic acids research · 2013Article
- Complex relationship between mismatch repair proteins and MBD4 during immunoglobulin class switch recombination.PloS one · 2013Article
- Simultaneous in vitro characterisation of DNA deaminase function and associated DNA repair pathways.PloS one · 2013Article
- Does DNA repair occur during somatic hypermutation?Seminars in immunology · 2012Review
- KAP1 regulates gene networks controlling mouse B-lymphoid cell differentiation and function.Blood · 2012Article
- Mismatch-mediated error prone repair at the immunoglobulin genes.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2011Review
- AID recruits UNG and Msh2 to Ig switch regions dependent upon the AID C terminus [corrected].Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Altered spectrum of somatic hypermutation in common variable immunodeficiency disease characteristic of defective repair of mutations.Immunogenetics · 2011Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Somatic hypermutation and class switch recombination (CSR) contribute to the somatic diversification of antibodies. It has been shown that MutS homologue (Msh)6 (in conjunction with Msh2) but not Msh3 is involved in generating A/T base substitutions in somatic hypermutation. However, their roles in CSR have not yet been reported. Here we show that Msh6(-)(/)(-) mice have a decrease in CSR, whereas Msh3(-)(/)(-) mice do not. When switch regions were analyzed for mutations, deficiency in Msh6 was associated with an increase in transition mutations at G/C basepairs, mutations at RGYW/WRCY hotspots, and a small increase in the targeting of G/C bases. In addition, Msh6(-)(/)(-) mice exhibited an increase in the targeting of recombination sites to GAGCT/GGGGT consensus repeats and hotspots in Sgamma3 but not in Smicro. In contrast to Msh2(-)(/)(-) mice, deficiency in Msh6 surprisingly did not change the characteristics of Smicro-Sgamma3 switch junctions. However, Msh6(-)(/)(-) mice exhibited a change in the positioning of Smicro and Sgamma3 junctions. Although none of these changes were seen in Msh3(-)(/)(-) mice, they had a higher percentage of large inserts in their switch junctions. Together, our data suggest that MutS homologues Msh2, Msh3, and Msh6 play overlapping and distinct roles during antibody diversification processes.
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