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

Fig. 2. A subset of proteins up-regulated by inhibition of mitochondrial respiration is required for longevity.

Fig. 2.

(A) Average percent changes in mean life span of WT and isp-1(qm150); ctb-1(qm189) [isp-1(−); ctb-1(−)] animals treated with each of 61 RNAi clones targeting genes that encode proteins whose levels were altered in both isp-1(qm150) [isp-1(−)] and clk-1(qm30) [clk-1(−)] mutants ≥2-fold. Yellow and blue circles indicate proteins with levels that were respectively increased and decreased by both isp-1(−) and clk-1(−). At least two independent life-span assays were conducted for each RNAi clone. Dotted lines, 10% life-span increase or decrease for WT or isp-1(−); ctb-1(−) animals. Circles with orange lines, significant results for both life-span trials. (B to D) RNAi targeting mon-2 (B), hrpu-2 (C), or patr-1 (D) significantly suppressed the long life span of isp-1(−) mutants. (E and F) mon-2(xh22) [mon-2(−)] mutations largely suppressed the longevity of isp-1(−) (E) and clk-1(−) (F) mutants (see the table S3 legends for the small or no effect of mon-2(−) on life span). (G to J) hrpu-2(tm1474) [hrpu-2(−)] and patr-1(gk155841) [patr-1(−)] mutations decreased the longevity of isp-1(−) (G and I) and clk-1(−) (H and J) mutants. (K) mon-2(−) suppressed the longevity of isp-1(−) animals without 5-fluoro-2′-deoxyuridine (FUDR) treatment. See also fig. S1 legends for discussion regarding the differences between our initial screen and the confirmation data. See table S2 for specific values and statistical analyses of the life-span data shown in this figure. LC-MS, liquid chromatography–mass spectrometry; m/z, mass/charge ratio.