The mpk-1(n2521) mutation suppressed the aex-2 RNAi-induced increase in protein degradation in muscle, as determined by LacZ staining, suggesting that the mpk-1 signaling pathway (Fibroblast Growth Factor pathway) is responsible for mediating the RNAi-induced increase in protein degradation in muscle.
The daf-18(e1375) mutation suppressed the aex-2 RNAi-induced increase in protein degradation in muscle, as determined by LacZ staining, suggesting that the daf-18 signaling pathway (Insulin-like signaling pathway) is responsible for mediating the RNAi-induced increase in protein degradation in muscle.
The unc-51(e369) mutation suppressed the aex-2 RNAi-induced increase in protein degradation in muscle, as determined by LacZ staining, suggesting that the unc-51 signaling pathway (Autophagy pathway) is responsible for mediating the RNAi-induced increase in protein degradation in muscle.
RNAi of T14B1.2 suppressed the reduction of ckb-2p::GFP expression resulting from the cdc-48.2(tm659) mutation, independent of ER-stress induced by tunicamycin
"we measured fluorescence intensity in cdc-48.2(-/-); ckb-2p::gfp worms fed with candidate RNAi clones and treated either with tunicamycin or vehicle (DMSO; Fig 1E). Seventy-seven RNAi clones showing a similar increase in the fluorescence ratios under both conditions were considered ER-stress independent and not further analyzed (Fig 1F, Supplementary Table S3)."
WT animals that express AEX-5::VENUS in the intestine, secrete AEX-5::VENUS, which accumulates in coelomocytes. In contrast, aex-4 mutants accumulate AEX-5::VENUS in intestinal cells and accumulate significantly less AEX-5::VENUS in coelomocytes.