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Transcription through immunoglobulin switch (S) regions is essential for class switch recombination (CSR), but no molecular function of the transcripts has been described. Likewise, recruitment of activation-induced cytidine deaminase (AID) to S regions is critical for CSR; however, the underlying mechanism has not been fully elucidated. Here, we demonstrate that intronic switch RNA acts in trans to target AID to S region DNA. AID binds directly to switch RNA through G-quadruplexes formed by the RNA molecules. Disruption of this interaction by mutation of a key residue in the putative RNA-binding domain of AID impairs recruitment of AID to S region DNA, thereby abolishing CSR. Additionally, inhibition of RNA lariat processing leads to loss of AID localization to S regions and compromises CSR; both defects can be rescued by exogenous expression of switch transcripts in a sequence-specific manner. These studies uncover an RNA-mediated mechanism of targeting AID to DNA.
Pubmed ID: 25957684
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Software package that integrates genome wide genetic variation with epigenetic data to identify collaborative transcription factor pairs. Optimized to work with chromatin accessibility assays such as ATAC-seq or DNase I hypersensitivity, as well as transcription factor binding data collected by ChIP-seq. Used to identify combinations of cell type specific transcription factors while simultaneously interpreting functional effects of non-coding genetic variation.
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