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. 2022 Feb 4;13:692. doi: 10.1038/s41467-022-28268-x

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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 AstC-R2::2A::GAL4-driven UAS-GFP expression (left, green) is apparent in the AKH-producing cells (APCs) of the CC, marked with anti-AKH (magenta). Images are representative of 8 tissues. Scale bars 20 μm. b Knockdown of AstC-R2 in the APCs phenocopies the starvation-survival effect of AstC knockdown in the gut; knockdown of AKH in these cells also reproduces this phenotype (p < 0.0001 by Kaplan–Meier log-rank test). c, d APC-specific knockdown of AstC-R2 reduces the consumption of TAGs (c) and glycogen (d) during starvation (two-way ANOVA genotype/diet interaction, p < 0.05; c: column 1 vs. 3, p < 0.0001; column 2 vs. 4, p < 0.0001; column 3 vs. 4, p = 0.0009; d: column 1 vs. 3, p < 0.0001; column 2 vs. 4, p < 0.0001; column 3 vs. 4, p < 0.0001). e, f Likewise, APC knockdown of AKH itself induces similar reductions in starvation-induced mobilization of TAGs (e) and glycogen (f). (e: column 1 vs. 3, p < 0.0001; column 2 vs. 4, p = 0.0002; column 3 vs. 4, p < 0.0001; f: column 1 vs. 3, p < 0.0001; column 2 vs. 4, p = 0.0002; column 3 vs. 4, p < 0.0001; all n = 10 except n = 9 for fed AKH>Dcr-2, n = 8 for starved AKH>Dcr-2. g The effects of AstC signaling are mediated by AKH: overexpressing AKH restores normal starvation sensitivity in animals with APC-specific knockdown of AstC-R2. h Likewise, overexpression of AKH in animals with APC-specific knockdown of AstC-R2 rescues their deficiency in lipid mobilization during starvation (column 1 vs. 3, p < 0.0001; column 3 vs. 4, p = 0.0055; all n = 10 except n = 9 for AKH > ). Error bars indicate standard error of the mean (SEM). ns, non-significant; and ***p < 0.001. Statistical significance was determined using Kaplan–Meier log-rank tests (b, g) or two-way ANOVA with Bonferroni’s post hoc test (c–f) or one-way ANOVA with Kruskal–Wallis test (h). Source data are provided as a Source data file.