Fig. 4

Elongator, components of AAG-initiated BER and AAG substrates accumulate towards the 3′end of co-regulated genes. a AAG ChIP-qPCR assays in HEK293T WT cells comparing percentage of input at gene bodies of unaffected gene (YTHDC1) and differentially expressed genes (ALDH1A2, CRMP1, CDH23, SYT9, and CDH4). b–e ChIP-qPCR assays showing relative AAG occupancy in AAG- and ELP1- dependent genes ALDH1A2 (b), CDH23 (c), CRMP1 (d), and unaffected gene YTHDC1 (e) in HEK293T WT cells. f–h ChIP-qPCR assays showing relative occupancy of HA-ELP1 in AAG- and ELP1- dependent ALDH1A2 (f), CDH23 (g), and CRMP1 (h) genes in HEK293T HA-ELP1cells. i–l ChIP-qPCR assays showing relative APE1 occupancy in negative control YTHDC1 gene (i), and AAG- and ELP1-dependent ALDH1A2 (j), CDH23 (k), CRMP1 (l) genes in HEK293T WT cells. m–p qPCR DNA damage assay showing differences in distribution pattern of aberrant AAG substrates in unaffected gene YTHDC1 (m) and genes regulated by AAG and ELP1: ALDH1A2 (n), CDH23 (o), CRMP1 (p) in HEK293T WT cells. Values are shown as relative occupancy: % input of specific gene region, relative to percentage input of promoter region. Error bars indicate mean ± SEM (n ≥ 3). Two-tailed Student’s t-test in a; one-way ANOVA in b–p; *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001. Source data are provided as Source Data file.