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. Author manuscript; available in PMC: 2015 Apr 2.
Published in final edited form as: Cell. 2013 Jan 31;152(3):417–429. doi: 10.1016/j.cell.2013.01.007

Figure 1. Repair of RAG-induced Antigen Receptor Locus DSBs by Classical Non-Homologous End Joining.

Figure 1

(A) RAG1 and −2 (yellow and orange ovals) are targeted to participating gene segments in the context of the 12/23 rule. Triangles represent 12-RSSs (blue) and 23RSSs (white) and boxes represent potential coding segments. (B) RAG holds cleaved hairpin coding and blunt RSS ends in a post-cleavage synaptic complex (PSC) and (C) directs the reaction into C-NHEJ initiated by Ku70 and Ku80 (dark and light purple ovals) binding. (D) Coding ends require processing and N regions can be added by TdT (grey oval) whereas (E) RSS ends are directly ligated by the XRCC4 (yellow oval)/Lig4 (red oval) complex to form coding and RSS joins, respectively. Functional redundancy of DDR and XLF in this reaction is indicated by ATM, 53BP1 and H2AX ovals separated by a line from an XLF oval. Specifically, coding joins are modestly impaired in the absence of the ATM and 53BP1 DDR factors and normal in the absence of the H2AX DDR factor or XLF C-NHEJ factor. However, coding joins are severely impaired in the combined absence of XLF and any one of the three DDR factors. RSS joins are normal in the absence of any one of the DDR factors or XLF but severely impaired in the absence of ATM or 53BP1 (H2AX was not tested) and XLF. See text for details.