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. 2021 Dec 3;7(49):eabj8156. doi: 10.1126/sciadv.abj8156

Fig. 5. mon-2 is required for longevity conferred by the inhibition of mitochondrial respiration via affecting autophagy.

Fig. 5.

(A) Confocal images of GFP::LGG-1/Atg8 in hypodermal seam cells of day 1 adult animals. mon-2(xh22) [mon-2(−)] mutations suppressed the increased number of GFP::LGG-1/Atg8-positive punctae in hypodermal seam cells of day 1 adult isp-1(qm150) [isp-1(−)] mutants but not in those of WT animals. Yellow arrows indicate punctae of GFP::LGG-1/Atg8. Scale bar, 5 μm. (B) Quantification of GFP::LGG-1 punctae in hypodermal seam cells of day 1 adults (n = 3, 30 animals per condition). Error bars represent SEMs (**P < 0.01, two-tailed Student’s t test). (C) mon-2 RNAi decreased the number of GFP::LGG-1 punctae in hypodermal seam cells in clk-1(qm30) [clk-1(−)] mutants at the L2-L3 larval stage (n = 3, 30 animals per condition). Error bars represent SEMs (**P < 0.01, two-tailed Student’s t test). (D and E) hlh-30 RNAi (D) or bec-1 RNAi (E) decreased the long life span of isp-1(−) animals but did not reduce the life span of isp-1(−) mon-2(−) animals. Unexpectedly, however, hlh-30 RNAi increased the level of MON-2::GFP in WT and isp-1(−) animals (fig. S4, L and M). We speculate that decreased autophagy caused by hlh-30 RNAi may up-regulate MON-2::GFP as a compensatory response. See table S6 for specific values and statistical analyses of the life-span data shown in this figure.