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. 2000 Mar;11(3):915–927. doi: 10.1091/mbc.11.3.915

Figure 8.

Figure 8

A mutation at residue Thr165 stabilizes Gcn4. (A) Pulse–chase analysis of wild-type (KB149) and mutant (KB854) Gcn4–LacZ expressed from the GAL promoter in W303 cells. Note the difference in time scale. (B) Expression of His4–LacZ from the full-length HIS4 promoter (plasmid pFN6; Nagawa and Fink, 1985). The strain used, bas1-2 bas2-2 gcn4Δ1 (KY26), is defective in both HIS4 transcription factors (Arndt et al., 1987). His4–LacZ expression is exclusively dependent on the plasmid-borne GCN4 alleles expressed from the ADE8 promoter of plasmids KB105 (WT) or KB853 (T165A). The β-galactosidase assay was performed as for Figure 7D.