Fig. 8: Impact of gut-derived Tk and AKH modulation on fecundity and lifespan in mated female flies.

a, Cumulative number of offspring measured over a 22-d period for controls (Tk^gut>) and females with EEC-specific RNAi against Tk (Tk^gut > Tk-RNAi; two-way ANOVA for genotype × day, followed by Fisher’s least significant difference test; for clarity, only P ranges are indicated here, with numerical values given in Extended Data Fig. 8a). b, Cumulative offspring count over 8 d for control females and animals undergoing TrpA1-mediated exogenous activation of Tk⁺ EECs, with and without simultaneous knockdown of Tk (two-way ANOVA for genotype × day with Dunnett’s test; numerical P values are given in Extended Data Fig. 8b). c, Fecundity assessment of female flies with knockdown of TkR99D or Akh in APCs (two-way ANOVA for genotype × day with Fisher’s least significant difference test; numerical P values are given in Extended Data Fig. 8c). d–g, Survival curves for female flies under the given dietary conditions. d, Lifespan of controls, animals with EEC-specific Tk knockdown and animals with TrpA1 activation of Tk⁺ EECs (with and without simultaneous Tk knockdown) on 10% and 20% yeast diets. e,f, Lifespan of animals with APC-specific knockdown of TkR99D (e) or Akh (f) on different dietary yeast concentrations. g, Longevity comparison between controls and gut-specific Tk-knockdown animals, both in an Akh-null background, on 20% and 10% yeast diets. h, Lifespan of animals with AkhR knockdown in all neurons (left, driven by R57C10-GAL4) or in fat tissue (right, with cg>), compared with their respective controls. i, A comprehensive model for Tk–SP regulation and function in mice and flies. a–c indicate mean ± s.e.m. Pairwise P values in d–h were obtained using log-rank (Mantel–Cox) tests. Sample sizes (n) and P values are indicated in each plot. In a–c, n represents independent groups of animals. d–h, n represents animals per group. NS, P > 0.05; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001.

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