Fig. 5
Lack of functional Elongator hampers AAG and APE1 chromatin recruitment, and AAG-initiated repair. a–d ChIP-qPCR experiments comparing AAG occupancy at promoters and gene bodies of ALDH1A2 (a), CRMP1 (b), CDH23 (c), and YTHDC1 (d) in HEK293T WT and ELP1−/− cells. e Immunoblot analysis of AAG levels in chromatin fraction of HEK293T WT and ELP1−/− cells. Histone H3 served as control. f Quantification of experiments as the one depicted in e. g ChIP-qPCR experiments comparing APE1 occupancy at gene bodies of YTHDC1, ALDH1A2, CRMP1, CDH23, SYT9, and CDH4 in HEK293T WT and ELP1−/− cells. Error bars represent the SEM calculated from at least three independent experiments. h Immunoprecipitation of AAG from HEK293T WT and ELP1−/− whole cell extracts showing the interaction with RNA polymerase II phosphorylated at Serine 2 (S2P) of CTD repeat. i Measurement of AAG DNA glycosylase activity in HEK293T WT, AAG−/− and ELP1−/− on hypoxanthine (Hx)-containing plasmid by FM-HCR assays. j AAG DNA glycosylase activity determined by FM-HCR assays on hypoxanthine (Hx)-containing plasmid in HEK293T WT cells complemented with GFP and AAG−/− cells complemented with GFP, GFP-AAG or GFP-Δ80 AAG. Error bars represent mean ± SEM (n ≥ 3). Two-tailed Student’s t-test (a–d, f, g); one-way ANOVA (i, j), NS – non significant, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001. Source data are provided as Source Data file.
