Fig. 4.
The atfs-1(gof) alleles protect C. elegans against prenylation inhibition. (A) Images of wild-type (WT), atfs-1(gk3094), and atfs-1(et15) worms cultivated for 96 h on control or gliotoxin (100 μM) plates. The gain-of-function atfs-1(et15) allele confers partial resistance to gliotoxin, whereas the loss-of-function atfs-1(gk3094) allele confers hypersensitivity as assessed by measuring growth (B) or viability (C) after 96 h on 100 μM gliotoxin. (D) The atfs-1(et15) allele can partially rescue the protein prenylation defects caused by fluvastatin. The protein prenylation reporter (pGLO-1P::GFP-CAAX) shows clear membrane enrichment in untreated L1 larvae for both wild-type and atfs-1(et15). In L1 larvae from parents cultivated in the presence of 0.5 mM fluvastatin for 48 h, only the atfs-1(et15) mutant continues to show membrane enrichment (white arrowheads). (E) Quantification of the prenylation assay using pGLO-1P::GFP-CAAX. The results are presented as the number of intestinal cells showing distinct membrane enrichment. Note that both atfs-1(et15) and atfs-1(et18) show a slight but significant increase in prenylation. (n > 35 worms; **P < 0.01, ***P < 0.001).