Figure 7.

Global genome NER model in wild-type versus XP-D/CS cells. While in WT cells the interaction between TFIIH and XPG allows a normal incision in 3′ of the lesion carrying DNA strand and the release of the CAK complex, in XP-D/CS cells, the weaker affinity between XPG and the TFIIH complex could significantly reduce the rate of successful incisions by the XPG endonuclease. This could then result in a DNA strand displacement mechanism, ultimately responsible for the advent of DNA breaks at later time points and the observed increased genomic instability. Moreover, in the presence of XPD^G602D, the CAK subcomplex does not seem to be properly released from TFIIH during GG-NER.