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. 2015 Oct 5;34(22):2789–2803. doi: 10.15252/embj.201591320

Figure 5. Swi6 dimerization and H3K9me2 binding are required for the prevention of H3K9me2 spreading.

Figure 5

  • A
    Domain architecture of full‐length Swi6. The indicated mutations in red disrupt the dimerization property of the CSD (L315E) or the ability of the CD to bind H3K9me2 (W104A).
  • B
    Schematic of the IRC1R boundary region. IRC1R partially overlaps with the region that expresses the noncoding RNA borderline (Keller et al, 2013). Positions of the quantitative RT–PCR primers are indicated in red.
  • C–E
    H3K9me2 levels on heterochromatin‐adjacent genes assessed by ChIP–PCR in swi6+, swi6∆, and swi6‐L315E (CSD dimerization mutant) (C), swi6‐W104A (H3K9me2 binding mutant) (D), and epe1∆ (E) cells. Enrichments over clr4∆ are normalized to adh1+. Average fold enrichment with s.d. is shown for three (C and E) or four (D) independent experiments. P‐values were generated by the Student's t‐test (two‐tailed distribution, two‐sample, unequal variance).