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. Author manuscript; available in PMC: 2017 Jul 17.
Published in final edited form as: Nature. 2016 Nov 30;540(7631):134–138. doi: 10.1038/nature20169

Figure 4. The GET and SND pathways act as backup for targeting in-vivo.

Figure 4

(a) Tetrads from Δsnd/Δget diploids demonstrate a synthetic sick/lethal interaction.

(b–d) Metabolic labeling of RFP-Gas1 (b), HA-Ysy6 (c) or DHCαF (d) showing decrease in translocated forms only for SRP-independent substrates in the conditional SND2/GET3 double-mutant. Accumulation of pre-inserted forms cannot be observed due to lack of proteasomal inhibition. Results repeated in three biological replicates.

(e) GFP fused to Gas1 GPI-anchoring sequence (GFP-ASGas1). Percentage of cells (from 100) with mistargeting depicted on images. Scale bar, 5 μm.

(f) Scheme of the eukaryotic ER-targeting apparatus.

(g) Model of the ER-targeting pathways’ interplay.

For gel source data see Supplementary Figure 1.