Fig. 3: Regulation of L1 source element activity. (IMAGE)
Caption
a, Schematic diagram of the multidimensional analysis. b, Panorama of DNA methylation status of 30 rc-L1s with developmental phylogenies for 132 normal colorectal clones and seven fibroblast clones from nine individuals. It includes 14 rc-L1s contributing any transduction events in these clones and 16 additional rc-L1s showing demethylated promoters in at least five clones. Numbers of branch-specific point mutations are shown in the phylogenies. c,d, DNA methylation status and readthrough transcription level of rc-L1 at 22q12.1-2 (c) and 12p13.32 (d). e, Proportion of non-truncation and promoter demethylation of 90 population-prevalent rc-L1s. Red dots, prevalent-active sources; black and grey dots, common sources showing any and no transduction events in our study, respectively. f, Differences in rc-L1 promoter methylation in clone pairs according to their embryonic branching time. The top 30 rc-L1s showing substantial variation in promoter methylation were considered. A fixed mutation rate4 was used to convert mutation time to embryonic cell generation. %P, percentage point; *P < 2.2 × 10−16 (two-sample Kolmogorov–Smirnov test). g,h, Methylation profile of 100 kb upstream and downstream regions of rc-L1 at 22q12.1-2 (g) and 1p12 (h). The rc-L1 loci are highlighted by yellow rectangles. Top, genomic coordinates and order of CpG sites. Middle, fraction of methylated CpG in colorectal (gold) and fibroblast (silver) clones (g), and in colorectal clones with open (orange) and closed (blue) promoters (h). Bottom, differences in fraction of methylated CpG depicted in middle panel. mCpG, methylated CpG.
Credit
none
Usage Restrictions
none
License
Original content