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. 2022 Nov 16;5:1255. doi: 10.1038/s42003-022-04212-z

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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. 8 — a L-methionine, b L-homocysteine, c L-cysteine, d L-glutathione and e L-taurine all require jnk-1, skn-1, daf-16 and sir-2.1 for their established health promoting effects on dys-1(eg33) movement capacity. Despite skn-1 co-treatments not presenting a significant decline in movement compared to untreated dys-1(eg33), the lack of movement preservation (as seen with the compounds alone) suggests each SAA requires full expression of this gene. All strains and conditions represent data from 10 animals with averages taken from 5 separate counts and repeated across three biological repeats. Results were analysed with a two-way ANOVA. Asterisks denote significance to untreated dys-1(eg33) animals. ***P < 0.0001, *P < 0.05, ns P > 0.05.