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. 2019 Sep 12;146(17):dev175315. doi: 10.1242/dev.175315

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© 2019. Published by The Company of Biologists Ltd

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Fig. 3. — GPDH1 controls NAD⁺/NADH redox balance during larval development. (A) Diagram illustrating how GPDH1 and LDH redundantly influence NAD⁺ levels. (B) GC-MS was used to measure relative G3P abundance in mid-L2 larvae for the following five genotypes (as presented left to right in the figure): Gpdh1^B18/+, Gpdh1^A10^/B18, Gpdh1^A10^/B18; da-GAL4/+, Gpdh^A10^/B18; UAS-Gpdh1 and Gpdh1^A10^/B18; da-GAL4 UAS-Gpdh1. (C) NAD⁺/NADH ratio in mid-L2 larvae of genotypes Gpdh1^B18/+, Ldh^16/17 and Gpdh1^A10^/B18. (D) Mid-L2 larvae were fed D-glucose-¹³C₆ for 2 h and the rates of ¹³C isotope incorporation into lactate and G3P were determined based on m+3 isotopologue abundance. (E) ATP levels were significantly decreased in Gpdh1^A10^/B18 compared with Gpdh1^B18/+ controls. (F) The body mass of Gpdh1^A10^/B18 larvae was significantly lower than that of Gpdh1^B18/+ controls 0-4 h after the L2-L3 molt. In B,C,E,F, n=6 biological replicates per genotype; in D, n=5 biological replicates per genotype. Error bars represent s.d. For B and C, the P-value was adjusted for multiple comparisons using the Bonferroni–Dunn method; ***P<0.001. All experiments were repeated a minimum of two times. G3P, glycerol-3-phosphate; DHAP, dihydroxyacetone phosphate; Lac, lactate.