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Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/30614

Title: The Mismatch Repair Pathway Functions Normally at a non-AID Target in Germinal Center B cells
Authors: Green, Blerta
Advisor: Martin, Alberto
Department: Immunology
Keywords: mismatch repair
somatic hypermutation
germinal center
activation induced cytidine deaminase
B cells
mutations
Issue Date: 7-Dec-2011
Abstract: Deficiency in Msh2, a component of the mismatch repair (MMR) system, leads to a ~10-fold increase in the mutation frequency in most tissues. By contrast, Msh2-deficiency in germinal center (GC) B cells decreases the mutation frequency at the IgH V-region, as a dU:dG mismatch produced by AID initiates modifications by MMR resulting in mutations at nearby A:T basepairs. This raises the possibility that GC B cells express a factor that converts MMR into a globally mutagenic pathway. To test this notion, we investigated whether MMR corrects mutations in GC B cells at a gene not mutated by AID. We found that GC B cells accumulate 5-times more mutations than follicular B cells. Notably, the mutation frequency was ~10 times higher in Msh2-/- compared to wildtype GC B cells. These results show that in GC B cells MMR functions normally at an AID-insensitive gene.
URI: http://hdl.handle.net/1807/30614
Appears in Collections:Master

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