Fig. 5
From: A fat-tissue sensor couples growth to oxygen availability by remotely controlling insulin secretion
Hypoxia and induction of hypoxia adaptation block growth and DILP secretion. a, b Quantification of pupal size (a) and representative images (b) of animals exposed to hypoxia (5% O2) or mutation of HIF-1a prolyl hydroxylase (Hph) compared with controls (w1118 in normoxia). Values are percent change in pupal size vs. w1118-in-normoxia controls. a: n = 24–34. c, d Transcript levels of Dilp genes in whole animals (c) and DILP peptide levels (d) in the insulin-producing cells (IPCs) of hypoxic wild-types and normoxic Hph mutants compared with normoxic wild types. Representative images of IPC DILP2, -3, and -5 immunostaining are shown below. c: n = 6. d: n = 29–42. e Hemolymph HA::DILP2::FLAG (DILP2HF) levels in normoxic (21% O2, on normal food), hypoxic (5% O2; normal food), and starved (21% O2; 1% agar) animals determined by ELISA. n = 5. f Immunoblotting shows that levels of phosphorylated Akt (pAkt) is reduced under hypoxia and in Hph mutants compared with btl > + controls when normalized to alpha-Tubulin (Tub) or total Akt levels. g tGPH reporter of insulin signaling confirms that hypoxia reduces systemic insulin signaling in peripheral tissues, represented here by the fat body. Under conditions of normal insulin activity (e.g., fed normoxia, left), the tGPH sensor is localized to the plasma membrane, whereas under conditions of low signaling (e.g., fed hypoxia, right) the sensor becomes primarily cytoplasmic. Scale bar, 20 µm. Statistics: one-way ANOVA with Dunnett’s multiple-comparisons test. *P < 0.05, **P < 0.01, ***P < 0.001, compared with the control. Error bars indicate SEM. Underlying data are provided in the Source Data file
