Fig. 3
From: A fat-tissue sensor couples growth to oxygen availability by remotely controlling insulin secretion
Breathless modulates systemic growth by altering DILP signaling. a Trachea-specific knockdown of breathless (btl) mimics loss of insulin signaling induced by ubiquitous InR knockdown (da > InR-RNAi) and fat-body inhibition of Tor (ppl > Tsc1/2), which remotely inhibits release of insulin-like peptides (DILPs) from the insulin-producing cells (IPCs). Values are percent change in pupal size vs. the btl > + controls (btl> crossed to w1118). n = 15–79. b, c Levels of whole-animal Dilp transcripts and DILP peptides in the IPCs in btl > btl-RNAi animals with knockdown of btl in the trachea compared with btl > + controls. Representative images of DILP2, -3, and -5 immunostainings are shown below. b: n = 5. c: n = 44–45. d Increased expression of InR in btl > btl-RNAi animals compared with btl > + controls suggests reduced systemic insulin signaling. n = 5. e, f Immunoblotting showing whole-animal levels of phosphorylated Akt (pAkt) (e) in btl > btl-RNAi animals compared with btl > + controls, quantified in f from three independent replicates normalized to Tubulin (Tub) or Akt levels. f: n = 3. g Ectopic expression of Dilp2 rescues the btl-knockdown size phenotype. Ubiquitous weak knockdown of btl using armadillo-GAL4 (arm > btl-RNAi) leads to small pupae (left). Co-expressing Dilp2 rescues this size phenotype (right), while having no significant effect on control animals (middle). Values are percent change in pupal size versus arm > + controls. n = 14–113. Statistics: one-way ANOVA with Dunnett’s test for multiple comparisons and Student’s t-test for pairwise comparisons. *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
