Figure 7. Model for UV-induced chromatin remodeling during GG-NER.

Top panel. In the absence of UV, basal levels of histone acetyl transferase occupancy are detected on the chromatin of the MFA2 promoter. The absence of histone acetyl transferase occupancy is marked by the presence of an inhibitory link. Consequently, histone H3 tails remain unacetylated and chromatin remains repressed. Lower Panel. Following UV the DNA translocase (1) and E3 ligase (2) activities of Rad16 in the GG-NER complex promote increased histone acetyl transferase occupancy on chromatin as indicated by the presence of arrows (3) and histone H3 acetylation (4) that drives chromatin remodeling as shown by a more open chromatin structure around the nucleosomes (5). Failure of the GG-NER complex to slide nucleosomes may prevent transcription factor binding explaining the continued repression of MFA2 transcription (6) despite chromatin remodeling. GG-NER dependent chromatin remodeling promotes efficient lesion removal (7).