Fig. 3: Longevity induced by dimt-1 deficiency requires the FoxO and TOR signaling pathways and requires an intact germline.
From: The 18S rRNA methyltransferase DIMT-1 regulates lifespan in the germline later in life
a Mutation of glutamic acid 79 to an alanine (E79A) in dimt-1 caused a complete elimination of 18S rRNA m6,2A as assessed by UHPLC-ms/ms. Statistics represent an unpaired two-tailed t-test with Welch’s correction. b Mutation of E79A in dimt-1 caused lifespan extension relative to WT worms. c dimt-1 knockdown extends the lifespan of both WT and eat-2(ad1116) mutant worm lifespan to a similar extent (p = 0.7021 by two-way ANOVA). d dimt-1 knockdown extends the lifespan of both WT and daf-2(e1370) mutant worm lifespan to a similar extent (p = 0.0806 by two-way ANOVA). e dimt-1 knockdown extends the lifespan of both WT and hsf-1(sy441) mutant worm lifespan to a similar extent (p = 0.4245 by two-way ANOVA). f dimt-1 knockdown extends the lifespan of WT but not daf-16(mu86) mutant worm lifespan (p < 0.0001 by two-way ANOVA). g dimt-1 knockdown extends the lifespan of WT but does not further extend the long lifespan of raga-1(ok386) mutant worms (p = 0.0327 by two-way ANOVA). h dimt-1 knockdown extends the lifespan of WT but does not further extend the long lifespan of germline deficient glp-1(e2141ts) mutant worms that were shifted to the restrictive temperature at the L1 stage (p < 0.0001 by two-way ANOVA). i dimt-1 knockdown extends the lifespan of WT but not sterile pgl-1(bn101ts) mutant worms whose mothers were shifted to the restrictive temperature (25.5 °C) at the L4 stage (p < 0.0001 by two-way ANOVA). Statistics and replicate experiments are presented in Supplementary Table 1. ns not-significant, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001 as calculated by log-rank (Mantel–Cox) statistical test.
