Chromatin-modifiying enzymes are essential when the Saccharomyces cerevisiae morphogenesis checkpoint is constitutively activated

Hs17p plays a central role in the morphogenesis checkpoint triggered when yeast bud formation is impaired and is proposed to function as an arginine methyltransferase. HSL7 is also essential in the absence of the N-terminal tails of histones H3 or H4. The requirement for H3 and H4 tails may indicate a need for their post-translational modification to bypass the morphogenesis checkpoint. In support of this, the absence of the acetyltransferases Gcn5p or Esa1p, the deacetylase Rpd3p, or the lysine-methyltransferase Set1p resulted in death or extreme sickness in hsl Delta mutants. These synthetic interactions involved both the activity of the chromatin-modifying enzymes and the complexes through which they act. Newly reported silencing phenotypes of hsl7 Delta mirror those previously reported for gcn5 Delta and rpd3 Delta, thereby strengthening their functional links. In addition, synthetic interactions and silencing phenotypes were suppressed by inactivation of the morphogenesis checkpoint, either by SWE1 deletion or by preventing Cdc28p phosphorylation. A catalytically dead Hs17p retained wild-type interactions, implying that modification of histone H3 or H4 N termini by Gcn5p, Esa1p, Rpd3p, and Set1p, but not by Hs17p, was needed to bypass the morphogenesis checkpoint.