Fig. 1: A role for exo-RNAi in ER homeostasis.
From: ER-associated RNA silencing promotes ER quality control
a, Turnover of the model substrate CPL‑1* via ERAD. b, Fluorescence images of worms expressing cpl‑1* with the indicated mutations and RNAi (empty control (Empty)) for the ERAD factor sel-11. c, Western blot of worm lysates corresponding to images shown in b, detecting CPL-1* (YFP) and tubulin (TUB). d, Fluorescence images of worms expressing cpl-1* with mutations in the exo-RNAi pathway. e, Western blot of worm lysates corresponding to the samples in d, detecting CPL-1* (YFP) and tubulin (TUB). f, Cellular fractionation of microsomes. Western blot detecting CPL-1* (YFP), CDC-48 (CDC-48) and SEL-1 (SEL-1). Pellet (P) and supernatant (SN) fractions of rde-1(ne219); cpl-1* worm lysates treated with the indicated chemicals after subcellular fractionation. g, Western blot of worm lysates detecting CPL-1* (YFP) and tubulin (TUB) in rde-1(ne219) worms and animals with intestinal Pnhx-2::rde-1 rescue. In b and d, pharyngeal expression of Pmyo-2::mCherry serves as transgenic marker. Scale bar, 200 µm. MW, molecular weight. Unprocessed blots are available in the source data.
