Insulin Signaling, Lifespan and Stress Resistance Are Modulated by Metabotropic GABA Receptors on Insulin Producing Cells in the Brain of Drosophila
Figure 5
GABAB receptor knockdown on IPCs increases sensitivity to starvation and desiccation.
We tested GABAB receptor knock-down with two Gal4 drivers, compared to parental controls, in starvation (flies kept on aqueous agarose) and desiccation (no food and no water). All experiments were run in at least three replicates, unless specified. A. Using a Dilp2-Gal4 driver to knock down the GABAB receptor (Dilp2-GBRi) we obtained flies that display significantly reduced survival at starvation (p<0.001, Log rank test; n = 210–270 for each genotype). B. The same genotypes were tested for survival during desiccation. (p<0.001; n = 120 for each genotype, 2 replicates). C. The OK107 Gal4 driver is also expressed in IPCs and was used for GABAB receptor knock-down (OK107-GBRi). At starvation survival is significantly decreased in OK107-GBRi flies (p<0.001; n = 155–193). D. The same genotypes were tested at desiccation. Again, a significant reduction was seen after receptor knockdown (p<0.001; n = 80–120; 2 replicates). E. As a control for the OK107 driver, that includes mushroom body Kenyon cells, we utilized a distinct driver for Kenyon cells (MB247) that is not expressed in median neurosecretory cells (IPCs). MB247-driven GBRi does not affect survival at starvation compared to the two parental controls (n = 100–184 for each genotype). F. We have no evidence for expression of the GABAA receptor subunit RDL in IPCs. Driving Rdl-RNAi in IPCs with the cross Dilp2-RdlRi did not alter survival at starvation. We found no significant difference between the three genotypes (n = 136–181; 2 replicates).