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. 2023 Jan 16;14:240. doi: 10.1038/s41467-023-35899-1

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© The Author(s) 2023

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. 2 — a The contents of NAD⁺ were increased in α-ketobutyrate (α-KB, 500 μM) -treated wild-type (WT) worms or glp-1(e2141ts) mutants. Knockdown of either cth-1 or cth-2 by RNAi reduced the levels of NAD⁺ in germline-deficient worms back to those of WT worms. Veh vehicle. Data were presented as mean values ± SEM of three independent experiments. P value was calculated using a one-way ANOVA followed by a Student–Newman–Keuls test. b RNAi knockdown of sir-2.1 inhibited lifespan extension by α-KB (500 μM) in WT worms. P values were calculated using a log-rank test. See survival statistics in Supplementary Data 1. Source data are provided as a Source Data file.