Figure 7

Model for the activity of TLK1/1B in translesion repair. Rad9 is known to be involved in translesion repair synthesis [34]. TLK1B helps modulating the activity and assembly of the 9-1-1 complex and promoting repair-coupled chromatin remodeling which depends on Asf1. Integration of the two activities is that TLK1/1B is first recruited to a DSB in a complex with 9-1-1 and the RFC-Rad17 clamp loader, to which Asf1 also binds [47]. At this point, TLK1/1B exchanges with Asf1 to promote nucleosomes eviction and access of the repair machinery to unencumbered DNA [11]. Faster repair can thus take place and is also followed by more rapid reassembly of chromatin, which is believed to be the real signal for resumption of the cell cycle [39]. We suggest that in DSB repair, Rad9 activity on ends-processing has an even more important role in repair [51].