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. Author manuscript; available in PMC: 2014 Dec 13.
Published in final edited form as: Nat Commun. 2014 Jun 13;5:4137. doi: 10.1038/ncomms5137

Figure 7. Model of the premature transcription termination as a source of ssDNA AID substrates.

Figure 7

The progression of Pol II reduces at the mutating Igh-V region, which leads to accumulation of stalling Pol II complexes (a, b). Most stalled Pol II complexes return to elongation after Pol II co-factor Spt5 recruits P-TEFb complexes that release pausing by phosphorylating C-terminal domains of both Spt5 and Pol II (c). However, non-resolvable pausing occurs stochastically, leading to premature transcription termination. Those early-terminated Pol II complexes leave unwound DNA region open with non-template ssDNA strand ready for AID targeting immediately (d). RPA complexes are then recruited to cover exposed non-template ssDNA while RNA:DNA hybrids are processed likely through nascent RNA removal process of transcription termination, which leaves single strand template DNA sensitive to AID (e). Partial transcripts are processed by the exosome complex, likely providing short RNA to in turn reduce Pol II progression at Igh-V and sustain the premature termination level there (f).