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Publication : Multiple transcription factor binding sites predict AID targeting in non-Ig genes.

First Author  Duke JL Year  2013
Journal  J Immunol Volume  190
Issue  8 Pages  3878-88
PubMed ID  23514741 Mgi Jnum  J:195285
Mgi Id  MGI:5477855 Doi  10.4049/jimmunol.1202547
Citation  Duke JL, et al. (2013) Multiple Transcription Factor Binding Sites Predict AID Targeting in Non-Ig Genes. J Immunol 190(8):3878-88
abstractText  Aberrant targeting of the enzyme activation-induced cytidine deaminase (AID) results in the accumulation of somatic mutations in approximately 25% of expressed genes in germinal center B cells. Observations in Ung(-/-) Msh2(-/-) mice suggest that many other genes efficiently repair AID-induced lesions, so that up to 45% of genes may actually be targeted by AID. It is important to understand the mechanisms that recruit AID to certain genes, because this mistargeting represents an important risk for genome instability. We hypothesize that several mechanisms combine to target AID to each locus. To resolve which mechanisms affect AID targeting, we analyzed 7.3 Mb of sequence data, along with the regulatory context, from 83 genes in Ung(-/-) Msh2(-/-) mice to identify common properties of AID targets. This analysis identifies three transcription factor binding sites (E-box motifs, along with YY1 and C/EBP-beta binding sites) that may work together to recruit AID. Based on previous knowledge and these newly discovered features, a classification tree model was built to predict genome-wide AID targeting. Using this predictive model, we were able to identify a set of 101 high-interest genes that are likely targets of AID.
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