Mismatch repair converts AID-instigated nicks to double-strand breaks for antibody class-switch recombination
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UMass Chan Affiliations
Department of Molecular Genetics and MicrobiologyDocument Type
Journal ArticlePublication Date
2006-01-01Keywords
AnimalsB-Lymphocytes
*Base Pair Mismatch
Cytidine Deaminase
*DNA Repair
Humans
*Immunoglobulin Class Switching
Mice
Models, Genetic
Recombination, Genetic
Life Sciences
Medicine and Health Sciences
Women's Studies
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Show full item recordAbstract
Mismatch repair (MMR) proteins are important for antibody class-switch recombination (CSR), but their roles are unknown. We propose a model for the function of MMR in CSR in which MMR proteins convert single-strand nicks instigated by activation-induced cytidine deaminase (AID) into the double-strand breaks (DSBs) that are required for CSR. This model does not invoke any novel functions for MMR but simply posits that, owing to numerous single-strand nicks in the switch (S) regions of both DNA strands, when MMR proteins are recruited by U:G mismatches, they excise one strand of DNA and soon reach a nick on the opposite strand. This halts excision activity and creates a DSB. This model explains why B cells that lack either S mu and MSH2 or UNG and MSH2 cannot undergo CSR.Source
Trends Genet. 2006 Jan;22(1):23-8. Epub 2005 Nov 23. Link to article on publisher's siteDOI
10.1016/j.tig.2005.11.002Permanent Link to this Item
http://hdl.handle.net/20.500.14038/50646PubMed ID
16309779Related Resources
Link to article in PubMedae974a485f413a2113503eed53cd6c53
10.1016/j.tig.2005.11.002