| Literature DB >> 26365193 |
Pilar M Dominguez1, Matt Teater2, Nyasha Chambwe3, Matthias Kormaksson4, David Redmond3, Jennifer Ishii5, Bao Vuong6, Jayanta Chaudhuri6, Ari Melnick1, Aparna Vasanthakumar7, Lucy A Godley7, F Nina Papavasiliou8, Olivier Elemento3, Rita Shaknovich9.
Abstract
Changes in DNA methylation are required for the formation of germinal centers (GCs), but the mechanisms of such changes are poorly understood. Activation-induced cytidine deaminase (AID) has been recently implicated in DNA demethylation through its deaminase activity coupled with DNA repair. We investigated the epigenetic function of AID in vivo in germinal center B cells (GCBs) isolated from wild-type (WT) and AID-deficient (Aicda(-/-)) mice. We determined that the transit of B cells through the GC is associated with marked locus-specific loss of methylation and increased methylation diversity, both of which are lost in Aicda(-/-) animals. Differentially methylated cytosines (DMCs) between GCBs and naive B cells (NBs) are enriched in genes that are targeted for somatic hypermutation (SHM) by AID, and these genes form networks required for B cell development and proliferation. Finally, we observed significant conservation of AID-dependent epigenetic reprogramming between mouse and human B cells.Entities:
Mesh：
Substances：
Year: 2015 PMID： 26365193 PMCID： PMC4591215 DOI： 10.1016/j.celrep.2015.08.036
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423