Fig. 5.

Fluvastatin and RNAi against HMG-CoA reductase induce the UPR via ire-1 and xbp-1. For panels A and B, worms of the strain SJ4005, which harbor the hsp-4::gfp transgene, were picked at the L3 stage and placed on control plates (A) or plates containing 1 mM fluvastatin (B) then photographed 24 h later. For panels C–E, worms of the strains SJ4005 (C), SJ17, which harbor the hsp-4::gfp transgene in a xbp-1 mutant background (D), and SJ30, which harbor the hsp-4::gfp transgene in a ire-1 mutant background (E) were grown for two generations on bacteria producing dsRNA against HMG-CoA reductase, then photographed at the L4 stage. In a separate experiment (lower row), RNAi against the M57.2 (annotated in Wormbase as a protein geranylgeranyl transferase type II, α subunit) caused the activation of the UPR reporter in strain SJ4005 (G), and this could not be rescued by supplementing the plates with mevalonate (H), farnesyl-pp (I), or geranylgeranyl-pp (J).