Figure 11.

Model for lesion recognition by CSB. Rad26 recognizes a stalled Pol II and can reduce its dwell time by preventing backtracking, promoting Pol II forward translocation on non-damaged templates, and increasing the chances of transcriptional bypass through less bulky DNA lesions, all of which stimulate transcription elongation. However, Rad26 fails to promote efficient transcriptional bypass of bulky DNA lesions that lead to strong blockage of translocation (such as CPD lesions). The interaction between Rad26 and a Pol II persistently arrested at a bulky lesion would lead to the initiation of TCR.