PAF1C-driven restoration of RNAPII elongation after DNA damage occurs independently of transcription-associated histone mark deposition

When RNAPII stalls on transcription-blocking lesions, the transcription-coupled DNA repair pathway is activated to remove the DNA damage. Following DNA repair, efficient transcription restart depends on the PAF1 elongation complex (PAF1C).

PAF1C contributes to deposition of transcription-associated histone marks, including H2B-K120Ub, H3K4me3 and H3K79me. These marks are enriched at actively transcribed genes and have been associated with regulation of post-repair transcription restart. Here, we show that the H2B-K120 E3 ubiquitin ligase RNF20/RNF40, the H3K4-methyltransferase SET1/COMPASS complex, and the H3K79-methyltransferase DOT1L are dispensable for transcription restart.