Furthermore, even though appearance of possibly Exo1 or Sgs1 restored normal HO-induced Rad53 hyperphosphorylation in mutant cells, the helicase-defective version of Sgs1 as well as the nuclease-defective version of Exo1 didn’t supplement this phenotype, indicating that the enzymatic actions of both protein are necessary for effective Rad53 activation

Furthermore, even though appearance of possibly Exo1 or Sgs1 restored normal HO-induced Rad53 hyperphosphorylation in mutant cells, the helicase-defective version of Sgs1 as well as…