Fig. 5

Lifespan extension due to utx-1 overexpression is independent of insulin signalling but at least partially dependent on daf-16. a Lifespan assays were performed on transgenic animals overexpressing utx-1 in a utx-1(tm3118) mutant background combined with daf-16 RNAi. daf-16 depletion significantly shortened the lifespan of wild-type and transgenic animals compared to EV controls (****p < 0.0001), although utx-1 overexpressing animals subjected to daf-16 RNAi did display a moderate lifespan extension compared to wild-type daf-16(RNAi) animals (****p < 0.0001). b Lifespan assays performed on daf-2(e1370) mutants subjected to utx-1 RNAi resulted in no significant change in survival compared with daf-2(e1370) EV controls, consistent with findings from [14]. The lifespan increase upon utx-1 RNAi in a wild-type background confirms that the utx-1 RNAi was working effectively. c Lifespan assays performed on daf-2(e1370) mutants compared to daf-2(e1370) mutants overexpressing utx-1 showed a significant lifespan extension compared with daf-2(e1370) mutants alone (**p = 0.0023) or utx-1 overexpression alone. EV, empty vector control (i.e. worms fed HT115 bacteria transformed with L4440 RNAi vector lacking a genomic insert); OE, overexpression (see Additional file 11: Table S7 for the full statistical analysis of lifespan data, including repeats)