Fig. 6. Two structures of TFIIH and schematic model of unwinding of DNA for NER.

A Ribbon representation of the yeast pre-unwound state (left) and previous structure of the human (artificially) unwound state (right, PDB:6RO4). Two structures are aligned by superimposing Ssl2 and XPB. B A model for unwinding damaged DNA by TFIIH, XPC, and XPA in NER. Lesion bound XPC is stabilized on TFIIH primarily through DNA-binding to XPB (left). XPC is then positioned near XPD for lesion scanning and verification by a concerted movement of XPD. The torque force by the translocase activity of XPB opens a bubble near damage, facilitating delivery of the damage DNA to XPD in an unwound form suitable for binding in the DNA-binding cleft (right). This unwinding step is also key to the lesion verification step in which a bulky lesion stalls and blocks the progression of XPD helicase unwinding, thereby allowing the incision complex to be stably formed. C A comparison between NER initiation (left) and Pol II transcription initiation (right). Two forms of TFIIH in NER initiation and transcription initiation are aligned. DNA in blue and green is rotated and translocated by Ssl2 in an ATP-dependent manner, in the directions indicated by the large red arrows.