Figure 6. Higher‐order structure changes in H3K27me3‐modified chromatin as detected by SAMMY‐Seq.

• A
  Representative Western blot on chromatin fractionation experiments of Ctrl and shMatr3 cells. Each fraction was loaded with the same number of cells. GAPDH, histone H3, Lamin A/C were used as positive controls for S1, S2 and S3, S4, respectively.
• B
  Genome browser view of the SAMMY‐Seq and H3K27me3 ChIP‐seq in Ctrl and shMatr3 (replicate 1 and 2 merged) cells at a representative region. Gray boxes under each SAMMY‐seq track showing the SAMMY‐seq domains. The shadows showing the shMatr3 loss SAMMY‐seq domains.
• C
  The genome coverage of SAMMY domains (S4. vs. S2) from AML12 cells. SAMMY domains are grouped into common, shMatr3‐lost and shMatr3‐gained domains by their genomic location between ctrl and shMatr3.
• D, E
  Average SAMMY‐seq signal (S4 vs. S2) (D) and average H3K27me3 ChIP‐seq signal (E) around SAMMY domains (groups as in C) with 200 kb upstream and downstream flanking regions of ctrl and shMatr3 from AML12 cells.
• F, G
  Average H3K27me3 ChIP‐seq signal (S4. vs. S2) (F) and average SAMMY‐seq signal (G) around H3K27me3 domains with 200 kb upstream and downstream flanking regions of ctrl and shMatr3 from AML12 cells. We calculate the overlapped region length between the H3K27me3 domains and three groups of SAMMY domains (same groups in [C]). For each H3K27me3 domain, the ratio of overlap regions (overlap length/H3K27me3 peak length) ≥ 0.6 was assigned to its overlapped SAMMY domains.
• H
  Average MATR3 RIP‐seq sense and antisense signal at L1 loci around H3K27me3 domains (groups as in [F]) with 200 kb upstream and downstream flanking regions from AML12 cells.
• I
  DEGs and the proportion of DEGs in relative to all genes in common, shMatr3‐lost and shMatr3‐gained SAMMY domains, respectively.
• J
  Histogram plots showing the DEGs number in 100 kb bins around SAMMY domains boundaries. Y‐axis is the DEGs number in each bin.

Source data are available online for this figure.