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. 2000 Oct;20(19):7214–7219. doi: 10.1128/mcb.20.19.7214-7219.2000

FIG. 1.

FIG. 1

Effect of cue1Δ, hrd1/der3Δ, and sec61-2 mutations on Ura3 fusion protein stability. (A) Growth without uracil of wild-type (WT), cue1Δ (3), and hrd1 der3Δ (6) cells carrying plasmids expressing fusion proteins with Ubc6p-Ubc7p-specific signals (11). pOC9 is the parent plasmid, which expresses stable Ura3p. Patches of mutant and isogenic wild-type cells were grown on SD plus uracil without tryptophan and replica plated onto SD without uracil and tryptophan. Growth on plates without uracil was taken as an indicator of Ura3p stability. (B) β-Galactosidase activity of sec61-2 mutant cells carrying plasmids expressing β-galactosidase (β-gal), the β-galactosidase-SL17 fusion protein (β-gal–SL17) (11), or β-galactosidase with an N-terminal lysine residue (K-β-gal) (2) at permissive and nonpermissive temperatures. (C) β-Galactosidase activity of wild-type and hrd1/der3Δ mutant cells carrying plasmids expressing β-galactosidase (β-gal), β-galactosidase-SL17 fusion protein (β-gal–SL17) (11), or β-galactosidase with an N-terminal lysine residue (K-β-gal) (2).