Figure S4.
Effect of ER exit motif mutations on Shr3-AAP interactions. Strains FGY135 (gap1Δ shr3Δ) expressing SHR3-NubA (pPL1262) and carrying pPL1257 (GAP1-Cub-GST), pIM19 (SSY1-Cub-GST), pIM28 (gap1-ERXAAA-Cub-GST), or pIM29 (ssy1-ERXAAA-Cub-GST) were induced with 2% galactose for 1 h. Extracts were prepared, separated by SDS-PAGE, and analyzed by immunoblotting using α-HA antibody. The signal intensities of the immunoreactive forms of full-length and cleaved Gap1 and Ssy1 constructs were quantified. The fraction of split-ubiquitin cleavage was determined; the mean values were plotted with error bars showing standard deviation (n = 3; biological replicates). Source data are available for this figure: SourceData FS4.

Effect of ER exit motif mutations on Shr3-AAP interactions. Strains FGY135 (gap1Δ shr3Δ) expressing SHR3-NubA (pPL1262) and carrying pPL1257 (GAP1-Cub-GST), pIM19 (SSY1-Cub-GST), pIM28 (gap1-ERXAAA-Cub-GST), or pIM29 (ssy1-ERXAAA-Cub-GST) were induced with 2% galactose for 1 h. Extracts were prepared, separated by SDS-PAGE, and analyzed by immunoblotting using α-HA antibody. The signal intensities of the immunoreactive forms of full-length and cleaved Gap1 and Ssy1 constructs were quantified. The fraction of split-ubiquitin cleavage was determined; the mean values were plotted with error bars showing standard deviation (n = 3; biological replicates). Source data are available for this figure: SourceData FS4.

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