The sex of specific neurons controls female body growth in Drosophila
Fig 5
Sex-lethal (Sxl) is required in insulin-producing cells (IPCs) and Gad1-Gal4 neurons to control sexual size dimorphism (SSD).
(A) Gal4-driver screen identifies 7 pan-neuronal, broad peptidergic (dimmc929, amon386Y), IPC (insulin-like peptide 2 [Ilp2]), and GABAergic* drivers with female-specific effects on body mass when combined with upstream activation sequence (UAS)-Sxl RNAi. For details and full results of screen, see S8 Fig. Left graph shows mean body mass and SD of 2–16 replicates of groups of 3–11 larvae. Hatched bars depict controls lacking the Sxl RNAi transgene, identified by the CyO, Dfd-YFP balancer, except for Gad1-Gal4 controls, which also include CyO, Dfd-YFP>Sxl RNAi larvae. In all cases, * p < 0.001 from respective no-driver controls using 2-way ANOVA with multiple comparisons. Right graph shows mean female to male (F:M) body mass ratios and SEMs for the Gal4 driver hits that decrease larval SSD. Expression analysis of elavc155-Gal4 and the other driver hits in this screen suggests that there is no shared secondary site of larval expression outside the nervous system (S1 Table). *Note that the 2 “GABAergic” drivers (Gad1-Gal4 and VGAT-Gal4) show only partially overlapping expression with GABA+ neurons (see S1 and S2 Images). (B) Ilp2-Gal4 and Gad1-Gal4 act additively to decrease female larval body mass via Sxl knockdown. Left graph shows mean body mass and SD of 3–4 replicates of groups of 6–10 larvae. Right graph shows mean F:M body mass ratios and SEMs. Knockdown of Sxl using both Ilp2-GAL4 and Gad1-Gal4 decreases female body mass and SSD more strongly than with each driver alone. Note that for Ilp2>Sxl RNAi and Ilp2 + Gad1>Sxl RNAi genotypes, results were pooled from 3 independent recombinants of Ilp2-Gal4, UAS-Sxl RNAi 1, each crossed to a no-driver control or to Gad1-Gal4, respectively. **** indicates p < 0.0001 using 1-way ANOVA with multiple comparisons. The underlying data for this figure can be found in S1 Data.