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• W1572851475 startingPage "1925" @default.
• W1572851475 abstract "Excision of uracil introduced into the immunoglobulin loci by AID is central to antibody diversification. While predominantly carried out by the UNG uracil-DNA glycosylase as reflected by deficiency in immunoglobulin class switching in Ung−/− mice, the deficiency is incomplete, as evidenced by the emergence of switched IgG in the serum of Ung−/− mice. Lack of switching in mice deficient in both UNG and MSH2 suggested that mismatch repair initiated a backup pathway. We now show that most of the residual class switching in Ung−/− mice depends upon the endogenous SMUG1 uracil-DNA glycosylase, with in vitro switching to IgG1 as well as serum IgG3, IgG2b, and IgA greatly diminished in Ung−/−Smug1−/− mice, and that Smug1 partially compensates for Ung deficiency over time. Nonetheless, using a highly MSH2-dependent mechanism, Ung−/−Smug1−/− mice can still produce detectable levels of switched isotypes, especially IgG1. While not affecting the pattern of base substitutions, SMUG1 deficiency in an Ung−/− background further reduces somatic hypermutation at A:T base pairs. Our data reveal an essential requirement for uracil excision in class switching and in facilitating noncanonical mismatch repair for the A:T phase of hypermutation presumably by creating nicks near the U:G lesion recognized by MSH2." @default.
• W1572851475 created "2016-06-24" @default.
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• W1572851475 date "2014-05-27" @default.
• W1572851475 modified "2023-09-23" @default.
• W1572851475 title "Uracil excision by endogenous <scp>SMUG</scp> 1 glycosylase promotes efficient <scp>I</scp> g class switching and impacts on <scp>A</scp> : <scp>T</scp> substitutions during somatic mutation" @default.
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• W1572851475 doi "https://doi.org/10.1002/eji.201444482" @default.
• W1572851475 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4158878" @default.
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• W1572851475 hasPublicationYear "2014" @default.
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