Fig. 9
From: Fear-of-intimacy-mediated zinc transport is required for Drosophila fat body endoreplication
The growth arrest, fat body developmental defects and blocked endoreplication in foi RNAi could be rescued by sod1 OE. A The increased expression of pJNK in Cg-Gal4 > foi RNAi larvae fat body was partially suppressed by sod1 OE. n = 40 fat bodies per group. B The decreased expression of Myc in foi RNAi larvae fat body could be significantly restored by sod1 OE. n = 40 fat bodies per group. C The smaller fat body size and cell size of Cg-Gal4 > foi RNAi were rescued by sod1 OE. n = 6 replicates per group. Scale bar, 100 μm. D Quantitative measurement of the fat body cell sizes in (C). (control, n = 104; Cg-Gal4 > foi RNAi, n = 84; Cg-Gal4 > foi RNAi, sod1 OE, n = 101; Cg-Gal4 > sod1 OE, n = 97 cells). E The eclosion defect of Cg-Gal4 > foi RNAi was significantly rescued by sod1 OE. n = 50–70 larvae per vial, n = 6 vials per experimental group. Genotypes used in (A-E) were Cg-Gal4 > w1118 (control), Cg-Gal4 > foi RNAi, Cg-Gal4 > foi RNAi, sod1 OE, Cg-Gal4 > sod1 OE. Data are represented as mean ± SEM of the biological replicates. ***p < 0.001; two-tailed Student’s t-test. F A model to explain the effect of zinc transporter FOI on Drosophila fat body endoreplication. Zinc transporter foi knockdown resulted in zinc deletion in the cytoplasm, leading to ROS accumulation and JNK activation, and subsequently inhibited the expression of Myc to block the DNA endoreplication in the fat body cell nucleus, then leading to fat body growth defect