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Changes in the locations and boundaries of heterochromatin are critical during development, and  de novo  assembly of silent chromatin in budding yeast is a well-studied model for how new sites of heterochromatin assemble.  De novo  assembly cannot occur in the G1 phase of the cell cycle and one to two divisions are needed for complete silent chromatin assembly and transcriptional repression. Mutation of  DOT1 , the histone H3 lysine 79 (K79) methyltransferase, and  SET1 , the histone H3 lysine 4 (K4) methyltransferase, speed  de novo  assembly. These observations have led to the model that regulated demethylation of histones may be a mechanism for how cells control the establishment of heterochromatin. We find that the abundance of Sir4, a protein required for the assembly of silent chromatin, decreases dramatically during a G1 arrest and therefore tested if changing the levels of Sir4 would also alter the speed of  de novo  establishment. Halving the level of Sir4 slows heterochromatin establishment, while increasing Sir4 speeds establishment.  yku70Δ  and  ubp10Δ  cells also speed  de novo  assembly, and like  dot1 Δ cells have defects in subtelomeric silencing, suggesting that these mutants may indirectly speed  de novo  establishment by liberating Sir4 from telomeres. Deleting  RIF1  and  RIF2 , which suppresses the subtelomeric silencing defects in these mutants, rescues the advanced  de novo  establishment in  yku70 Δ and  ubp10 Δ cells, but not in  dot1Δ  cells, suggesting that  YKU70  and  UBP10  regulate Sir4 availability by modulating subtelomeric silencing, while  DOT1  functions directly to regulate establishment. Our data support a model whereby the demethylation of histone H3 K79 and changes in Sir4 abundance and availability define two rate-limiting steps that regulate  de novo  assembly of heterochromatin.

Competition between Heterochromatic Loci Allows the Abundance of the Silencing Protein, Sir4, to Regulate de novo Assembly of Heterochromatin