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. 2022 Jun 9;24(6):906–916. doi: 10.1038/s41556-022-00926-8

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© The Author(s) 2022

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — a, Relative levels of FFAs, saturated fatty acids (SFAs), MUFAs and PUFAs are quantified by liquid chromatography–mass spectrometry in lipl-4 Tg versus WT. b, Percentage of lipid species showing significant changes (P < 0.05) in the lysosome purified from lipl-4 Tg versus WT worms. Out of 186 TAG species decreased in lipl-4 Tg, 117 contain PUFAs. Sphingophospholipids (SPH), phosphatidylcholines (PC), lysophosphatidylcholines (LPC), phosphatidylethanolamines (PE), lysophosphatidylethanolamines (LPE), phosphatidylserines (PS), lysophosphatidylserines (LPS), phosphatidylinositols (PI), diacylglycerols (DAG) and TAG. c, Schematic diagram of PUFA biosynthesis in C. elegans. PUFAs enriched in lipl-4 Tg are highlighted in blue, while desaturase enzymes are marked in green. d, The loss-of-function mutation of the fatty acid desaturase fat-1(lf) or fat-3(lf) suppresses the transcriptional upregulation of egl-3 and egl-21 neuropeptide genes by lipl-4 Tg. e,f, RNAi knockdown of either fat-1 (e) or fat-3 (f) selectively in the intestine suppresses lipl-4 Tg longevity. In a, error bars represent mean ± s.e.m., n = 6 (WT) and n = 9 (lipl-4 Tg) biologically independent samples, *P = 0.028 for C18:4n3, P = 0.023 for C14:0 and P = 0.026 for C15:0, **P = 0.007 for C18:2n6 and P = 0.002 for C18:3n3/6, ****P < 0.0001 for C16:1n7, C20:2n6, C20:3n6 and C20:4n6 by two-way ANOVA with Holm–Sidak correction (lipl-4 Tg versus WT), ~40,000 worms per replicate. In d, error bars represent mean ± s.e.m., n = 4 (WT, fat-1(lf), fat-3(lf) and lipl-4 Tg;fat-1(lf)) and n = 3 (lipl-4 Tg and lipl-4 Tg;fat-3(lf)) biologically independent samples, ***P < 0.001 by two-way ANOVA with Holm–Sidak correction, ~3,000 worms per replicate. In e and f, n = 3 biologically independent samples, ***P < 0.001 by log-rank test, 60–120 worms per replicate. See Supplementary Table 5 for full lifespan data. Source numerical data are available in source data.

Source data