Fig. 5: RSF1 KO impairs p300 binding and the subsequent histone H3 acetylation on p53-target promoters.

a ChIP analysis of histone p300 at the promoters of CDKN1A (p21, numbers: see Fig. 4) and BBC3 (PUMA, middle, numbers: see Fig. 4), and p53 response elements of BAX, and PMAIP1 (NOXA, the locations: see Fig. 4). The enrichment of p300 on these promoters after treatment with etoposide was calculated and represented in % input. NS not significant. b The level of enrichment of p300 at the promoters after treatment with etoposide in RSF1 KO cells was normalized to the level before treatment in control cells. NS not significant. c ChIP analysis of histone H3 acetylation (H3ac) at the promoters of BBC3 (PUMA). The enrichment of histone H3 acetylation on these promoters after treatment with etoposide was calculated and represented in % input. d The level of enrichment of histone H3 acetylation at the promoters after treatment with etoposide in RSF1 KO cells was normalized to the level before treatment in control cells. e Luciferase assay to measure p53 activity for transcriptional regulation upon DNA damage. The activity of p53 for transcription was measured in the condition of p300 or RSF1 deficiency, as well as double deficiency of p300 and RSF1 after etoposide treatment. PG13 contains 13 repeats of p53 binding sites, and MG15 contains 15 repeats of the mutated binding site. NS not significant