FIG. 4.

Summary of screen to identify eIF2α mutants with defects in GCN4 translational control, eIF2α phosphorylation, or eIF2B binding. The indicated eIF2α residues were subjected to site-directed or random mutagenesis, and the mutated alleles were screened in yeast to identify mutations that blocked growth on 3-AT medium and thus eliminated GCN4 regulation (second column). Yeast strains expressing the eIF2α alleles that blocked growth on 3-AT medium were also tested for phosphorylation of Ser51 (see Fig. 5), and mutations that eliminated or reduced Ser51 phosphorylation in vivo are listed in the third column. Mutations that conferred a 3-AT^s phenotype but did not impair Ser51 phosphorylation were tested for eIF2B binding (see Fig. 7), and mutations that eliminated or reduced eIF2B binding are listed in the last column. Mutations previously reported (27) to impair the binding of eIF2B to phosphorylated eIF2α are also listed (italicized and underlined) in the last column.