Extended Data Fig. 9: POLD2, ADAR1, FEN1, and PRIM1 exhibit elevated occupancy at centromeres.
From: Redox-driven ADAR1 activation promotes Okazaki fragment maturation and DNA replication integrity
(a) Occupancy of POLD2, ADAR1, FEN1 and PRIM1 evaluated for each 100k bins relative to their distance to centromeres. (b) Genome-wide distribution of peaks for POLD2, PRIM1, ADAR1, and FEN1. Bars in the top panel represent the density of peaks per 5 Mb (y-axis: number of peaks per 5 Mb window). Centromere regions are indicated by pink shades on each chromosome. Bars in the bottom panel represent group-scaled ChIP-seq signals (y-axis: normalized read depth) along chromosome 4, with the red dotted square indicating the centromere region. (c) Distribution of signal across chromosome Y and chromosome 20 in the Pol α-RNR mutant after Pu-seq (y-axis: normalized read density, arbitrary units). The red dotted boxes indicate centromere regions. Three biological replicates are shown. (d) The peak span of the Pol α-RNR mutant within sub-centromere regions was compared to an equal number of peaks randomly sampled from other genomic regions. SC refers to sub-centromeres and RR refers to random regions. 60 events quantified in each condition are shown. Data are mean ± SDs. A two-tailed unpaired t-test was performed to assess the statistical significance of peak size differences between the two groups.
