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. 2014 May 19;111(22):E2271–E2280. doi: 10.1073/pnas.1318262111

Fig. 6.

Fig. 6.

mdt-15 inactivation and defects in PL biosynthesis activate the UPRER without compromising ER protein quality control. (A) The plots show the survival of adult control(RNAi), mdt-15(RNAi), ire-1(RNAi), WT, mdt-15(tm2182), ire-1(zc14), SCD(RNAi), and sams-1(RNAi) worms on 30 μg/mL tunicamycin. The P values for mdt-15(tm2182) and sams-1(RNAi) worms indicate resistance. One of at least three independent experiments is shown; for additional replicates, see Fig. S4A. (B) Bar graphs represent the fractions of L1/L2, L3, or L4 stage control(RNAi), mdt-15(RNAi), and SCD(RNAi) larvae that are alive after 48 h on 0, 2, or 5 μg/mL tunicamycin (Upper) or on 0, 3, or 5 μg/mL thapsigargin (Lower). One of three independent experiments is shown. (C, Left) The average number of hatched F1 progeny per individual P0 WT or ire-1(zc14) worm grown on control, enpl-1, mdt-15, SCD, or sams-1 RNAi. (Right) The ratio of hatched progeny from ire-1(zc14) mutants over WT worms for each RNAi treatment. n = 4; error bars represent SEM; *P < 0.05 as determined by two-tailed unpaired Student t test. Micrographs below the bar graphs show WT or ire-1(zc14) worms carrying the hsp-4p::GFP reporter on control, enpl-1, mdt-15, SCD, or sams-1 RNAi. (D) Micrographs depict worms expressing the hsp-4p::GFP reporter on control or sams-1 RNAi with or without 30 mM ethanolamine or choline supplementation (Left and Center) and on SCD RNAi without supplementation (no supplement), with C18:1n-9 supplementation (oleate), with C18:2 and C20:5 supplementation (PUFAs), or with C18:1n-9, C18:2, and C20:5 supplementation (O+PUFAs) (Right). One of three independent experiments is shown.