AID targeting is dependent on RNA polymerase II pausing.
Activation induced deaminase (AID) is globally targeted to immunoglobulin loci, preferentially focused to switch (S) regions and variable (V) regions, and prone to attack hotspot motifs. Nevertheless, AID deamination is not exclusive to Ig loci and the rules regulating AID targeting remain unclear. Transcription is critically required for class switch recombination and somatic hypermutation. Here, I consider the unique features associated with S region transcription leading to RNA polymerase II pausing, that in turn promote the introduction of activating chromatin remodeling, histone modifications and recruitment of AID to targeted S regions. These findings allow for a better understanding of the interplay between transcription, AID targeting and mistargeting to Ig and non-Ig loci.
Department of Microbiology and Immunology, University of Illinois College of Medicine, 835 S. Wolcott, Chicago, IL 60612-7344, USA. star1@uic.edu
Amy L
AL
Kenter
D000818:Animals; D003564:Cytidine Deaminase / Q000235:genetics / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D009154:Mutation; D011485:Protein Binding; D012319:RNA Polymerase II / Q000378:metabolism*; D050436:Regulatory Elements, Transcriptional; D014158:Transcription, Genetic; D000098830:AICDA (Activation-Induced Cytidine Deaminase)
D012319:RNA Polymerase II; D000098830:AICDA (Activation-Induced Cytidine Deaminase); D003564:Cytidine Deaminase