Skip to main content
. Author manuscript; available in PMC: 2016 Sep 17.
Published in final edited form as: Mol Cell. 2015 Sep 17;59(6):1025–1034. doi: 10.1016/j.molcel.2015.08.012

Figure 7. A Model of Tripartite Lesion Recognition and Verification.

Figure 7

(A) TFIIH is associated with chromatin weakly in a non-specific manner without DNA lesion.

(B) In the presence of DNA lesions (red hexagon), TFIIH is loaded onto the DNA by XPC or RNA Pol II in a strand- and orientation-specific manner. It scans both DNA strands in parallel with XPD and XPB helicases.

(C) Translocation of TFIIH on normal DNA is accelerated by XPA. Small base lesions and mismatches (small red triangle), which are substrates for base excision and mismatch repair, respectively, behave like normal DNA.

(D) Upon detection of a bulky lesion (red star) on the strand scanned by XPD, both XPB and XPD helicases are stalled by the lesion. XPA enhances the stalling and hence bulky-lesion recognition. After dissociation of CAK, Core7, RPA, and XPA stabilize the bubble structure around the lesion and recruit XPF and XPG to make sequential dual incisions. Repair-coupled DNA synthesis can facilitate incision by XPG and lesion removal.