Fig. 3

Freeze–thaw stress-induced morphologic cell defects blocked by daf-2(rf). Adult animals were treated with freeze–thaw stress as described in the Methods; after 6 h of recovery, surviving animals were scored for cell morphology. All GFP reporter genes [40] were stably integrated. Every assay was repeated three times (n > 12–21) in the same conditions. Nuclear-localized pmyo-3:gfp reporter gene expression in body wall muscle nuclei. PD4251 (A, a), daf-2 RNAi (C, c), [daf-16(mgDf47); daf-2(e1370)] (E, e), age-1 RNAi (G, g), or pdk-1 RNAi (I, i) animals not exposed to freeze–thaw stress treatment were observed. PD4251 (B, b) and [daf-16(mgDf47); daf-2(e1370)] (F, f) animals’ nuclear GFP expression was fragmented (arrow) with freeze–thaw stress. Additionally, daf-2 RNAi (D, d), age-1 RNAi (H, h), and pdk-1 RNAi (J, j) animals had preserved nuclear morphology with freeze–thaw stress