The CSD amino acid composition in Swi6-WT permits binding to effector proteins that inhibit (Epe1) and promote (Clr3 and rixosome) heterochromatin, leading to restriction of heterochromatin maintenance at the ectopic locus. Upon Swi6-Y mutation, the Epe1 interaction is lost and the rixosome interaction is upregulated, leading to enhanced heterochromatin maintenance. Upon Swi6-K mutation, the Epe1 interaction is lost but the rixosome interaction is not upregulated, leading to defective heterochromatin maintenance. Swi6-Y and Swi6-K are more chromatin-bound than Swi6-WT, indicating the chromatin landscape is altered. The rixosome is recruited to heterochromatin directly by Swi6 for heterochromatin RNA clearance. Chromatin-associated transcripts are processed for subsequent degradation, allowing for Clr4-mediated read-write heterochromatin inheritance. Therefore, our findings support a model where Swi6-mediated effector recruitment, specifically Epe1 and the rixosome, influences epigenetic inheritance of heterochromatin.
