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Activation‐induced cytidine deaminase auto‐activates and triggers aberrant gene expression
Author(s) -
Isobe Tomoyasu,
Song Soken-Nakazawa J.,
Tiwari Prabha,
Ito Hiroki,
Yamaguchi Yuki,
Yoshizaki Kazuyuki
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.06.028
Subject(s) - activation induced (cytidine) deaminase , cytidine deaminase , dna demethylation , ectopic expression , dna methylation , epigenetics , biology , gene expression , regulation of gene expression , reporter gene , gene , microbiology and biotechnology , genetics , somatic hypermutation , b cell , antibody
DNA methylation is a well‐characterized epigenetic landmark involved in transcriptional regulation; however, mechanisms underlying its regulation remain poorly characterized. Recent studies demonstrate that activation‐induced cytidine deaminase (AID) is involved in active DNA demethylation. AID is aberrantly expressed in inflammation‐associated cancers and generates point mutations; however, cellular disorders attributed to its demethylation function are largely unexplored. Here we demonstrate that ectopic AID expression perturbs tumor‐related gene expression. AID (with Gadd45) activated a methylated paired box gene 5 (Pax5) reporter construct, and induced expression and association of endogenous Pax5 with the AID promoter, suggesting that aberrant AID expression triggers an auto‐activation circuit to consolidate self‐expression.