Fig. 6: Working model of the coordination of TCR and repair-independent release of lesion-stalled Pol II in response to TBLs. | Nature Communications

Fig. 6: Working model of the coordination of TCR and repair-independent release of lesion-stalled Pol II in response to TBLs.

From: Coordination of transcription-coupled repair and repair-independent release of lesion-stalled RNA polymerase II

Fig. 6: Working model of the coordination of TCR and repair-independent release of lesion-stalled Pol II in response to TBLs.

Left: For cells with deficiencies in CSB or CSA gene that are related to CS, Pol II cannot be ubiquitinated, thus both TCR and p97-driven Pol II release are blocked, resulting in extended retention of Pol II on damage sites. Middle: For cells with mutated UVSSA which can cause UVSS, TCR is also blocked due to the lack of UVSSA or deficiency in TFIIH loading. However, Pol II (and CSB) can be ubiquitinated, so p97 can remove lesion-stalled Pol II to prevent its accumulation. Right: For normal cells with proficient TCR, p97 would not access ubiquitinated Pol II during TCR, thus cannot interfere with repair. Lesion-stalled Pol II should be resolved mainly by TCR.

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