Fig. 6: PG-specific signaling inhibition after the NRC impairs mitochondrial homeostasis and causes developmental arrest.
From: Nutrient status alters developmental fates via a switch in mitochondrial homeodynamics
A–D PG-specific inhibition of PTTH signaling, insulin signaling, and TORC1 after the NRC impairs mitochondrial homeostasis. Representative images of mitochondrial morphology A, green, colocalization of Dib-mCherry (red) and mitochondria (mito-GFP, green) B, mitophagy C, and proteasomal activity D, red in the PG (168 h AEL) with knockdown of Torso, InR, and Torso + InR, or expression of RasDN, Dp110DN, TORDN and TSC1/2. A n = 24 (Control), 20 (Torso-RNAi), 21 (RasDN), 20 (InR-RNAi), 23 (Dp110DN), 24 (Torso+InR-RNAi), 21 (TORDN), 27 (TSC1/2). B n = 30 (Control), 29 (Torso-RNAi), 23 (RasDN), 34 (InR-RNAi), 19 (Dp110DN), 21 (Torso+InR-RNAi), 34 (TORDN), 23 (TSC1/2). C n = 28 (Control), 20 (Torso-RNAi), 19 (RasDN), 34 (InR-RNAi), 30 (Dp110DN), 27 (Torso+InR-RNAi), 28 (TORDN), 26 (TSC1/2). E, F PG-specific inhibition of PTTH, insulin, and TORC1 signalings after the NRC causes developmental arrest. Developmental timing with the indicated genotypes was examined under feeding conditions. n = 22 (Control), 8 (Torso-RNAi), 16 (RasDN), 12 (InR-RNAi), 15 (Dp110DN), 15 (Torso+InR-RNAi), 19 (TORDN), 11 (TSC1/2). Data are presented as mean ± SD. The genotypes and statistical data are provided in Supplementary Data 1.
